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Posted: Thu May 01, 2008 11:56 pm
by gibbledygook
Getting dressed this morning I quite unconsciously lifted my right leg without aid onto my left knee, slightly bent the toes to ease entry of the shoe. It all felt really natural. But normally I have to lift my right leg with my hands and I don't bend the foot to ease the passage of the foot. Probably a one-off.

Posted: Tue May 06, 2008 6:15 am
by gibbledygook
I have received my 2 packs of lauricidin and I am going to add 1 scoop twice daily. I will be particularly interested to see if this has any effect on the arthritis which developed recently in my right index finger. So far 18g of curcumin has not altered the pain in my right finger so I think there may be bacterial involvement. If the lauricidin packs don't do much I shall try triphala, the ayurvedic combination which looks effective for certain types of arthritis.
1: Vascul Pharmacol. 2008 Jan;48(1):14-20. Epub 2007 Nov 13. Links
An in vivo and in vitro potential of Indian ayurvedic herbal formulation Triphala on experimental gouty arthritis in mice.Sabina EP, Rasool M.
School of Bio-engineering and Biosciences, VIT University, Vellore-632 014, Tamil Nadu, India.

In the present study, we have investigated the efficacy of Indian ayurvedic herbal formulation Triphala on monosodium urate crystal-induced inflammation in mice; an experimental model for gouty arthritis and compared it with that of the non-steroidal anti-inflammatory drug, Indomethacin. The anti-arthritic effect of Triphala was evaluated by measuring changes in the paw volume, lysosomal enzyme activities, lipid peroxidation, anti-oxidant status and inflammatory mediator TNF-alpha in control and monosodium urate crystal-induced mice. The levels of beta-glucuronidase and lactate dehydrogenase were also measured in monosodium urate crystal-incubated polymorphonuclear leucocytes (PMNL). Triphala treatment (1 gm/kg/b.w. orally) significantly inhibited the paw volume and the levels of lysosomal enzymes, lipid peroxidation and inflammatory mediator tumour necrosis factor-alpha; however the anti-oxidant status was found to be increased in plasma, liver and spleen of monosodium urate crystal-induced mice when compared to control mice. In addition, beta-glucuronidase and lactate dehydrogenase level were reduced in Triphala (100 microg/ml) treated monosodium urate crystal-incubated polymorphonuclear leucocytes. In conclusion, the results obtained clearly indicated that Triphala exerted a strong anti-inflammatory effect against gouty arthritis
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1: Phytother Res. 2007 Sep;21(9):889-94. Links
Antiinflammatory effect of the Indian Ayurvedic herbal formulation Triphala on adjuvant-induced arthritis in mice.Rasool M, Sabina EP.
School of Bio-engineering and Biosciences, Vellore Institute of Technology, Deemed University, Vellore 632 014, Tamil Nadu, India. mkr474@rediffmail.com

In the present study, attempts have been made to evaluate the antiarthritic effect of the Indian Ayurvedic herbal formulation Triphala on adjuvant-induced arthritis in mice and to compare it with that of the non-steroidal antiinflammatory drug indomethacin. Arthritis was induced by intradermal injection of complete Freund's adjuvant (0.1 mL) into the right hind paw of Swiss albino mice. Triphala (1 g/kg/bxwt) and indomethacin (3 mg/kg/bxwt) were administered orally for 8 days (from day 11 to 18) after adjuvant injection. The levels of lysosomal enzymes, tissue marker enzymes, glycoproteins and paw thickness were increased in adjuvant-induced arthritic animals. The body weight was found to be reduced when compared with the control animals. These physical and biochemical changes observed in arthritic animals were altered significantly to near normal conditions after oral administration of Triphala (1 g/kg/bxwt). The results obtained clearly indicate the fact that the Indian Ayurvedic herbal formulation Triphala has promising antiinflammatory activity.
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Perhaps especially formulations containing myrrh:
1: J Biosci. 2007 Jun;32(4):755-61. Links
Hyaluronidase and collagenase inhibitory activities of the herbal formulation Triphala guggulu.Sumantran VN, Kulkarni AA, Harsulkar A, Wele A, Koppikar SJ, Chandwaskar R, Gaire V, Dalvi M, Wagh UV.
Interactive Research School for Health Affairs (IRSHA), Bhartiya Vidyapeeth Deemed University Medical College Campus, Dhankawadi, Pune 411 043, India. venils@hotmail.com

Myrrh (guggulu) oleoresin from the Commiphora mukul tree is an important component of antiarthritic drugs in Ayurvedic medicine. Clinical data suggest that elevated levels of hyaluronidase and collagenase type 2 enzymes contribute significantly to cartilage degradation. Triphala guggulu (TG) is a guggulu-based formulation used for the treatment of arthritis. We assessed the chondroprotective potential of TG by examining its effects on the activities of pure hyaluronidase and collagenase type 2 enzymes. Triphala shodith guggulu (TSG), an intermediate in the production of TG, was also examined. A spectrophotometric method was used to assay Hyaluronidase activity, and to detect potential Hyaluronidase inhibitors. Aqueous and hydro-alcoholic extracts of TSG showed weak but dose-dependent inhibition of hyaluronidase activity. In contrast, the TG formulation was 50 times more potent than the TSG extract with respect to hyaluronidase inhibitory activity. A validated X-ray film-based assay was used to measure the gelatinase activity of pure collagenase type 2. Hydro-alcoholic extracts of the TG formulation were 4 times more potent than TSG with respect to collagenase inhibitory activity. Components of Triphala were also evaluated for their inhibitory activities on hyaluronidase and collagenase. This is the first report to show that the T2 component of Triphala (T.chebula) is a highly potent hyaluronidase and collagenase inhibitor. Thus, the TG formulation inhibits two major enzymes that can degrade cartilage matrix. Our study provides the first in vitro preclinical evidence of the chondroprotective properties of TG.
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1: Curr Opin Pharmacol. 2007 Jun;7(3):344-51. Epub 2007 May 1. Links
Natural products as a gold mine for arthritis treatment.Khanna D, Sethi G, Ahn KS, Pandey MK, Kunnumakkara AB, Sung B, Aggarwal A, Aggarwal BB.
Division of Immunology, Department of Medicine, University of Cincinnati, Cincinnati, OH, USA.

Arthritis, an inflammation of the joints, is usually a chronic disease that results from dysregulation of pro-inflammatory cytokines (e.g. tumour necrosis factor and interleukin-1beta) and pro-inflammatory enzymes that mediate the production of prostaglandins (e.g. cyclooxygenase-2) and leukotrienes (e.g. lipooxygenase), together with the expression of adhesion molecules and matrix metalloproteinases, and hyperproliferation of synovial fibroblasts. All of these factors are regulated by the activation of the transcription factor nuclear factor-kappaB. Thus, agents that suppress the expression of tumour necrosis factor-alpha, interleukin-1beta, cyclooxygenase-2, lipooxygenase, matrix metalloproteinases or adhesion molecules, or suppress the activation of NF-kappaB, all have potential for the treatment of arthritis. Numerous agents derived from plants can suppress these cell signaling intermediates, including curcumin (from turmeric), resveratrol (red grapes, cranberries and peanuts), tea polyphenols, genistein (soy), quercetin (onions), silymarin (artichoke), guggulsterone (guggul), boswellic acid (salai guggul) and withanolides (ashwagandha). Indeed, several preclinical and clinical studies suggest that these agents have potential for arthritis treatment. Although gold compounds are no longer employed for the treatment of arthritis, the large number of inexpensive natural products that can modulate inflammatory responses, but lack side effects, constitute 'goldmines' for the treatment of arthritis.
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Posted: Wed May 07, 2008 3:11 am
by gibbledygook
I've made the switch to the more bioavailable forms of curcumin from Life Extension. Each 400mg allegedly is worth 2.7g of typical maximised types. I am taking 800mg every 2 hours and my legs are feeling GOOD! I really am astonished at how effective a solid dose of curcumin is on my MS. It's like a form of steroids or something! MIND you, I keep forgetting that I started taking boswellia at the same time that I upped the dose of curcumin so maybe that has something to do with my improvement.
My arthritic finger is still painful in the morning but I think maybe the pain has been diminishing somewhat so it'll be hard to know if the lauricidin is doing anything. This is a question I've often wondered with all of the other supplements I take except curcumin. The list of supplements is becoming somewhat ludicrous. I am now taking 7.2g of the bioavailable curcumin, about 3g of green tea, 3g of ganoderma lucidum plus the other chinese herbs in the tea, reservatrol 800mg, magnolia, boswellia, vitamin b,c,d,e, quercetin, gotu kola, grape seed extract, lauricidin, inosine, magnesium, calcium, alpha lipoic and maybe more. The heat is on in London with the 2nd of a glorious sunny 20degrees C and the wisteria is all out. Yet my walking is not a disaster and there is a spring in my step. I would put this down almost entirely to the curcumin as most of the data for most of the other compounds are in significantly higher doses than I am taking. I'm quite interested in ramping up consumption of gotu kola and boswellia but steady as she goes....! :lol:

Posted: Wed May 07, 2008 5:07 am
by jak7ham9
Dear Gobbledygook. I am on the abx wheldon/stratton protocol and unlike your not so good experience I am quite pleased so far no progression. My mri Has cleared dramatically and I look and feel well. My only thing not really improved so far (I have been on 6 month) is the tightness and gait issues. I read about your high circumin helping with that. So i am going to give it a shot. Mine is always tied in with inflammation. When the inflammation decreases my walking improves immediately.I will let you know how it goes. Barbara thanks :)

Posted: Wed May 14, 2008 2:39 am
by gibbledygook
Good luck Jak7, bear in mind that my walking was pretty terrrible; only 2 months ago my EDSS was 6.5 and I could barely manage 5 meters! Yesterday, a sunny 20 degrees C or so with low humidity, I managed another 700 meters walking with a very tall friend. The last 100 meters were a bit of a struggle and I needed her arm. This is somehow rather disappointing as I had been hoping to go seamlessly from strength to strength in my walking and other symptoms. Still I've only been on the really high dose of curcumin since the end of April. I guess after 4 years of poor walking it might take longer than 2 weeks to be able to walk again normally! But I don't think I'm EDSS 6.5 any more, maybe more like 5 or 4.5.
I have added bioperine 30mg a day which I hope might aid the absorption of the boswellia which is also tricky to get through the gut, like curcumin. Unfortunately I can't see any especially bioavailable forms of boswellia at Iherb .
The arthritic pain in my right index finger is still noticeable in the mornings but has definitely improved since the end of April. Whether this is the now 3 scoops of lauricidin or not is rather hard to know. The lauricidin certainly hasn't stopped the pain.

I have ordered a triphala/guggul combination from an ayurvedic website just to see if that helps clear this pain up as well. I think maybe these anti-inflammatories will assist better than licorice/magnolia/reservatrol/green tea/sambucol anti-virals which I continue to take but which didn't have a very noticeable effect until I upped the curcumin dose. Confusingly I now realise that I started the boswellia when I increased the curcumin so I now no longer know for sure that it was the increased dose of curcumin that has been so effective. Maybe it's the increased dose of curcumin AND the boswellia which are being so effective. :oops:

So I shall see what, if anything, happens when I remove a supplement from my regimen. :D This will happen next week when I go away to sunny Mallorca for a week. I shall only pack the curcumin and bioperine so it will be interesting to see if missing the boswellia has an effect.

15/5/2008 I moderate somewhat the intake of curcumin but increase somewhat the boswellia. I now take 6 800mg (4,600mg) of curcumin a day spaced out by 3 hours, 6 10mg of bioperine, 6 source naturals boswellia (total of 1,572 mg)and 6 life extension 5-loxi boswellia ( a total of 450mg). I take all of this with the bioperine to aid absorption and with a hot chinese tea where possible, after about half an hour and when possible I try to eat a quite fatty food.
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1: Planta Med. 2004 Dec;70(12):1155-60. Links
Effect of food intake on the bioavailability of boswellic acids from a herbal preparation in healthy volunteers.Sterk V, Büchele B, Simmet T.
Department of Pharmacology of Natural Products & Clinical Pharmacology, University of Ulm, Ulm, Germany.

In this study we investigated the effects of concomitant food intake on the bioavailability of distinct boswellic acids (BAs) from the test preparation BSE-018, a dry extract from Boswellia serrata gum resin. In a randomised, open, single-dose, two-way crossover study, healthy male subjects received three capsules of BSE-018 equivalent to 786 mg dry extract of Boswellia serrata gum resin either in the fasted state or together with a standardised high-fat meal. BA plasma concentrations were analysed for up to 60 h after oral dosing by reversed phase HPLC. As compared to the fasted state (treatment A), the administration of BSE-018 concomitantly with a high-fat meal (treatment B) led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA), 11-keto-beta-boswellic acid (KbetaBA) and acetyl-11-keto-beta-boswellic acid (AKbetaBA). Plasma levels of both acetyl-alpha-boswellic acid (AalphaBA) and alphaBA became only detectable when administered with treatment B, i.e., the high-fat meal. Accordingly, pharmacokinetic data could be calculated for betaBA, KbetaBA and AKbetaBA (treatment A) and for betaBA, KbetaBA, AKbetaBA, alphaBA, and AalphaBA (treatment B). For the first time these data reveal detailed kinetics of BAs after oral dosing of an extract and demonstrate a profound effect of food intake on the pharmacokinetic profile of the BAs. This finding should be very important whenever BAs would be considered for therapeutic use
19/5/2008
I didn't like taking so much boswellia especially after yesterday's early morning dose which was followed by quite bad foot cramps, something I've not really had before. So I'm backing off to 3 x the source naturals and 3 x the 5 loxin a day. I also noticed over the weekend an increased stiffness in the right leg and around the left knee. This is better today on less boswellia or is it just better weather? Looks pretty humid out there today.
One thing's for sure GRAZAX is fantastic for my hayfever. I have hardly sneezed all summer. Usually by the time of the chelsea flower show I am struggling. So at least some medicines work!

20/5/2008
Today I go it alone with the curcumin and bioperine. This is to ascertain what is helping and what is not. I think both curcumin and boswellia are helpful but I'm not sure so I'm just going to take the curcumin and black pepper extract for a couple of weeks to see if I improve/decline and add herbs back in one by one.

19:31 I managed 700 meters today after 1.5 glasses of red but with my cane. My bladder was rather poor after the wine and coffee and this affected my walking until I got to the toilet. mmm. I think I like the curcumin only trial.

only curcumin

Posted: Wed May 28, 2008 7:46 am
by gibbledygook
I have stopped nearly all my supplements including nac and acidophilus and inosine to ascertain what, if anything, is having a good effect. I completed a week of curcumin alone, taking 3 pills of the maximised life extension brand every 3 hours with a bioperine pill to aid absorption. On the whole I felt that there was a very slight increase in tingling particularly around the left knee compared with curcumin AND boswellia. Mind you I was in a more humid and wine orientated environment (it poured with rain in mallorca and there was a good wine list and a lot of football matches...). I therefore stared taking boswellia again yesterday with a dose of 1 source naturals and 1 life extension brand 3 times daily with the curcumin and bioperine. Today my leg feels less tingly and less stiff but this is probably just placebo effect! Today I have also started my new chinese tea, the constituents of which are, in order of importance: gentianae macrophyllae radix, liquidambaris fructus, alismatis rhizoma, ginseng radix, achyranthis bidentatae, scutelleriae radix, ban xia (can't find the translation), glycerrhizae and bupleuri radix. I see that in my chinese medicine bible the gentian is said to complement boswellia.

I have also received some ayurvedic supplements, called guggul plus, for my arthritic finger, which annoyingly now seems quite a bit better than it was. The ingredients of each capsule is terminalia arjuna 63mg, piper longum 42mg, zingiber officinale 42mg, piper nigrum 42mg, emblica officinalis 42mg, terminalia chebula 42mg, terminalia belerica 42mg, trigonella foenum-graecum 4mg, curcuma longa 42mg, commiphor mukul 21mg. I shall leave this a week to see how the boswellia and chinese tea play out on the curcumin mainstay.
My leg feels a lot better than it was a few months ago but wasn't terribly good in mallorca which was very humid and hilly and hungover.
Inhibitory effects of the Gentiana macrophylla (Gentianaceae) extract on rheumatoid arthritis of rats

Farong Yua, 1, Fahong Yub, 1, Rende Lic, , and Rui Wangc, ,

aGansu Institute of Political Science and Law, Lanzhou 730070, China

bDepartment of Biochemistry and Molecular Biology, University of Florida, Gainesville, FL 32610, USA

cSchool of Life Sciences, Lanzhou University, Lanzhou 730000, China


Received 20 August 2003; revised 24 March 2004; accepted 29 June 2004. Available online 14 August 2004.




References and further reading may be available for this article. To view references and further reading you must purchase this article.


Abstract
Acute treatment of rheumatoid rats with an extract from the roots of Gentiana macrophylla (Gentianaceae) produced a significant inhibitory effect on rheumatoid arthritis (RA). When rats were administered the Gentiana macrophylla extract orally at a daily dose of 100 mg/kg body weight, the prostaglandin E2 (PGE2) levels in the inflammatory tissues, sole thickness, and ankle circumferences of feet were significantly decreased. The anti-inflammatory activity observed in Gentiana macrophylla is comparable to that observed in prednisone. These observations suggest that Gentiana macrophylla displays considerable potency in anti-inflammatory action and could be used as an anti-inflammatory agent in the control of inflammation of rheumatoid arthritis
1: Zhong Xi Yi Jie He Za Zhi. 1989 Mar;9(3):156-7, 133-4.Links
[Observation on the treatment of systemic lupus erythematous with a Gentiana macrophylla complex tablet and a minimal dose of prednisone][Article in Chinese]


Yuan ZZ, Feng JC.
Sixty-two cases of systemic lupus erythematous (SLE) treated with Tab. Gentiana macrophylla complex 5 tablets three times per day or 10 tablets twice per day and prednisone 10-30 mg per day were reported. As controls, 19 cases of SLE were treated with prednisone alone at the same time. The results showed complete remission in 86.46% (50/62) cases in the observation group and 31.57% (6/19) cases in the control group. Eight cases of SLE treated with Tab. Gentiana m. complex alone also achieved complete remission in 6 cases and improvement in 2. There was very significant statistical difference between the two groups (P less than 0.001). The Tab. Gentiana m. complex was more effective on the improvement of nephropathy, arthralgia, erythema and restoration of ESR, LE cells and CH50, C3 than prednisone alone. No apparent side effects of Tab. Gentiana m. complex were found in this observation.
also looking for herbs to repair leads to...
1: Brain Res. 2006 Dec 6;1123(1):68-79. Epub 2006 Oct 31. Links
Catalpol increases hippocampal neuroplasticity and up-regulates PKC and BDNF in the aged rats.Liu J, He QJ, Zou W, Wang HX, Bao YM, Liu YX, An LJ.
Department of Bioscience and Biotechnology, School of Environmental and Biological Sciences, Dalian University of Technology, 2 Linggong Road, Dalian, Liaoning 116024, PR China.

Rehmannia, a traditional Chinese medical herb, has a long history in age-related disease therapy. Previous work has indicated that catalpol is a main active ingredient performing neuroprotective effect in rehmannia, while the mechanism underlying the effect remains poorly understood. In this study, we attempt to investigate the effect of catalpol on presynaptic proteins and explore a potential mechanism. The hippocampal levels of GAP-43 and synaptophysin in 3 groups of 4 months (young group), 22-24 months (aged group) and catalpol-treated 22-24 months (catalpol-treated group) rats were evaluated by western blotting. Results clearly showed a significant decrease in synaptophysin (46.6%) and GAP-43 (61.4%) levels in the aged group against the young animals and an increase (45.0% and 31.8% respectively) in the catalpol-treated aged rats in comparison with the untreated aged group. In particular, synaptophysin immunoreactivity (OD) in the dentate granule layer of the hippocampus was increased 0.0251 in the catalpol-treated group as compared with the aged group. The study also revealed a catalpol-associated increase of PKC and BDNF in the hippocampus of the catalpol-treated group in comparison with the aged rats and highly correlated with synaptophysin and GAP-43. Such positive correlations between presynaptic proteins and signaling molecules also existed in the young group. These results suggested that catalpol could increase presynaptic proteins and up-regulate relative signaling molecules in the hippocampus of the aged rats. Consequently, it seemed to indicate that catalpol might ameliorate age-related neuroplasticity loss by "normalizing" presynaptic proteins and their relative signaling pathways in the aged rats.
more stuff on boswellia:
1: Wien Med Wochenschr. 2002;152(15-16):373-8.Links
[Boswellic acids (components of frankincense) as the active principle in treatment of chronic inflammatory diseases][Article in German]


Ammon HP.
Lehrstuhl Pharmakologie für Naturwissenschaftler, Pharmazeutisches Institut der Universität Tübingen, Deutschland. sekretariat.ammon@uni-tuebingen.de

Preparations from the gum resin of Boswellia serrata have been used as a traditional remedy in Ayurvedic medicine in India for the treatment of inflammatory diseases. Compounds from the gum with genuine antiinflammatory effects are pentacyclic triterpenes of the boswellic acid type. Boswellic acids inhibit the leukotriene biosynthesis in neutrophilic granulocytes by a non-redox, noncompetitive inhibition of 5-lipoxygenase. The effect is triggered by boswellic acids binding to the enzyme. Moreover certain boswellic acids have been described to inhibit elastase in leukocytes, to inhibit proliferation, induce apoptosis and to inhibit topoisomerases of leukoma- and glioma cell lines. A series of chronic inflammatory diseases are thought to be perpetuated by leukotrienes. In clinical trials promising results were observed in patients with rheumatoid arthritis, chronic colitis, ulcerative colitis, Crohn's disease, bronchial asthma und peritumoral brains edemas.
1: Nutr Clin Pract. 2008 Feb;23(1):49-62. Links
A review of complementary and alternative approaches to immunomodulation.Clarke JO, Mullin GE.
Division of Gastroenterology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. gmullin1@jhmi.edu

Current Western therapies for inflammatory diseases are suboptimal; increasingly, patients are turning to complementary and alternative medicine for symptom relief and improved quality of life. There is emerging evidence that many of these therapies have the ability to modulate the immune system and disrupt the proinflammatory cascade through a variety of mechanisms, including antioxidant effects, alterations in cell signaling (in particular the nuclear factor (NF)-kappaB pathway), cytokines, proinflammatory mediators, and disruption of bacterial flora. Using inflammatory bowel disease (IBD) as a model of inflammation, we explore the principal complementary and alternative medicine treatments that show promise in this regard, namely, resveratrol, green tea, curcumin, boswellia, fish oil, vitamin D, and probiotics. With each agent, we detail the mechanisms that have been described with regard to immune modulation, discuss the medical conditions for which it has been evaluated, and explore the data to date for the prevention or treatment of IBD.
1: Mol Pharmacol. 2007 Dec;72(6):1657-64. Epub 2007 Sep 25. Links
Incensole acetate, a novel anti-inflammatory compound isolated from Boswellia resin, inhibits nuclear factor-kappa B activation.Moussaieff A, Shohami E, Kashman Y, Fride E, Schmitz ML, Renner F, Fiebich BL, Munoz E, Ben-Neriah Y, Mechoulam R.
Department of Medicinal Chemistry and Natural Products, Medical Faculty, Hebrew University, Jerusalem 91120, Israel. ariehm@ekmd.huji.ac.il

Boswellia resin is a major anti-inflammatory agent in herbal medical tradition, as well as a common food supplement. Its anti-inflammatory activity has been attributed to boswellic acid and its derivatives. Here, we re-examined the anti-inflammatory effect of the resin, using inhibitor of nuclear factor-kappaB alpha (IkappaB alpha) degradation in tumor necrosis factor (TNF) alpha-stimulated HeLa cells for a bioassay-guided fractionation. We thus isolated two novel nuclear factor-kappaB (NF-kappaB) inhibitors from the resin, their structures elucidated as incensole acetate (IA) and its nonacetylated form, incensole (IN). IA inhibited TAK/TAB-mediated IkappaB kinase (IKK) activation loop phosphorylation, resulting in the inhibition of cytokine and lipopolysaccharide-mediated NF-kappaB activation. It had no effect on IKK activity in vitro, and it did not suppress IkappaB alpha phosphorylation in costimulated T-cells, indicating that the kinase inhibition is neither direct nor does it affect all NF-kappaB activation pathways. The inhibitory effect seems specific; IA did not interfere with TNFalpha-induced activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase. IA treatment had a robust anti-inflammatory effect in a mouse inflamed paw model. Cembrenoid diterpenoids, specifically IA and its derivatives, may thus constitute a potential novel group of NF-kappaB inhibitors, originating from an ancient anti-inflammatory herbal remedy.
1: Int J Colorectal Dis. 2007 Dec;22(12):1445-51. Epub 2007 Sep 2. Links
Boswellia serrata extract for the treatment of collagenous colitis. A double-blind, randomized, placebo-controlled, multicenter trial.Madisch A, Miehlke S, Eichele O, Mrwa J, Bethke B, Kuhlisch E, Bästlein E, Wilhelms G, Morgner A, Wigginghaus B, Stolte M.
Medical Department I, Technical University Hospital, Fetscherstrasse 74, 01307, Dresden, Germany. ahmed.madisch@uniklinikum-dresden.de

BACKGROUND AND AIMS: The objective of this study was to investigate the effect of Boswellia serrata extract (BSE) on symptoms, quality of life, and histology in patients with collagenous colitis. MATERIALS AND METHODS: Patients with chronic diarrhea and histologically proven collagenous colitis were randomized to receive either oral BSE 400 mg three times daily for 6 weeks or placebo. Complete colonoscopy and histology were performed before and after treatment. Clinical symptoms and quality of life were assessed by standardized questionnaires and SF-36. The primary endpoint was the percentage of patients with clinical remission after 6 weeks (stool frequency<or=3 soft /solid stools per day on average during the last week). Patients of the placebo group with persistent diarrhea received open-label BSE therapy for a further 6 weeks. RESULTS: Thirty-one patients were randomized; 26 patients were available for per-protocol-analysis. After 6 weeks, the proportion of patients in clinical remission was higher in the BSE group than in the placebo group (per protocol 63.6%; 95%CI, 30.8-89.1 vs 26.7%, 95%CI, 7.7-55.1; p=0.04; intention-to-treat 43.8% vs 26.7%, p=0.25). Compared to placebo, BSE treatment had no effect on histology and quality of life. Five patients discontinued BSE treatment prematurely. Discontinuation was due to adverse events (n=1), unwillingness to continue (n=3), or loss to follow-up for unknown reasons (n=1). Seven patients received open-label BSE therapy, five of whom achieved complete remission. CONCLUSIONS: Our study suggests that BSE might be clinically effective in patients with collagenous
1: Int Immunopharmacol. 2007 Apr;7(4):473-82. Epub 2007 Jan 8. Links
Pure compound from Boswellia serrata extract exhibits anti-inflammatory property in human PBMCs and mouse macrophages through inhibition of TNFalpha, IL-1beta, NO and MAP kinases.Gayathri B, Manjula N, Vinaykumar KS, Lakshmi BS, Balakrishnan A.
Centre for Biotechnology, Anna University, Chennai, India.

The aim of the present study is to probe the anti-inflammatory potential of the plant Boswellia serrata by studying the effect of the crude extract and the pure compound isolated from it on key inflammatory mediators like TNFalpha, IL-1beta, and NO thus enabling the understanding of the key signaling events involved. The crude methanolic extract and the pure compound were analysed for their inhibitory effect on TNFalpha, IL-1beta and IL-6. The results demonstrated that all three cytokines are down regulated when PBMCs are cultured in the presence of crude extract or the pure compound at various time points. Observations on Th1/Th2 cytokines revealed marked down regulation of Th1 cytokines IFNgamma and IL-12 while the Th2 cytokines IL-4 and IL-10 were up regulated upon treatment with crude extract and pure compound. The extract and the pure compound isolated also showed considerable inhibition of NO production in activated RAW 264.7 cells, possibly via suppression of inducible NO synthase mRNA expression. Further to elucidate the underlying mechanism of action the effect of 12-ursene 2-diketone on LPS-induced activation of MAPK has also been examined. Our results demonstrated that 12-ursene 2-diketone inhibits the expression of pro-inflammatory cytokines and mediators via inhibition of phosphorylation of the MAP kinases JNK and p38 while no inhibition was seen in ERK phosphorylation in LPS-stimulated PBMCs. The above study therefore indicates that the crude methanolic extract and the isolated pure compound are capable of carrying out a natural anti-inflammatory activity at sites where chronic inflammation is present by switching off the pro-inflammatory cytokines and mediators, which initiate the process.
1: J Clin Rheumatol. 2004 Oct;10(5):236-245. Links
A 32-Week Randomized, Placebo-Controlled Clinical Evaluation of RA-11, an Ayurvedic Drug, on Osteoarthritis of the Knees.Chopra A, Lavin P, Patwardhan B, Chitre D.
From the *Center for Rheumatic Diseases, Inlaks and Budhrani Hospital, Bharati Hospital Medical College (Deemed University), Pune, India; †Averion, Inc., Framingham, Massachusetts; the ‡School of Health Sciences, University of Pune, India; and §BIO-VED Pharmaceuticals, Inc., San Jose, California.

BACKGROUND:: The ancient Indian (Asian) Ayurvedic medicinal system uses herbomineral drugs to treat arthritis. Despite centuries of use, very few have been tested by drug trials. RA-11 (ARTREX, MENDAR), a standardized multiplant Ayurvedic drug (Withania somnifera, Boswellia serrata, Zingiber officinale, and Curcuma longa) is currently used to treat arthritis. OBJECTIVE:: The objective of this study was to evaluate the efficacy and safety of RA-11 in patients with symptomatic osteoarthritis (OA) of the knees. METHODS:: A total of 358 patients with chronic knee pain were screened free-of-cost in "arthritis camps" in an Indian metropolis. Ninety patients with primary OA of the knees (ACR classification; Arthritis Rheum 1986;29:1039-1049) were found eligible (postanalgesic washout pain visual analog score [VAS] >/=40 mm in either or both knees on body weight-bearing activities) to enroll into a randomized, double-blind, placebo-controlled, parallel efficacy, single-center, 32-week drug trial (80% power to detect 25% difference, P = 0.05, 2-sided). Concurrent analgesics/nonsteroidal antiinflammatory drugs and steroids in any form were not allowed. Lifestyle and/or dietary restrictions, as per routine Ayurveda practices, were not imposed. Pain VAS (maximum pain in each knee recorded by the patient during the preceding 48 hours) and modified WOMAC (Western Ontario McMaster University OA Index, Likert scale, version 3.0) were the primary efficacy variables. The WOMAC section on "physical function difficulty" was modified for Indian use and validated before the trial. Routine laboratory testing was primarily done to monitor drug safety. At baseline, the groups (active = 45, placebo = 45) were well matched for several measures (mean pain VAS: active = 6.17; placebo = 6.5). RESULTS:: 1) Efficacy: Compared with placebo, the mean reduction in pain VAS at week 16 (active = 2.7, placebo = 1.3) and week 32 (active = 2.8, placebo = 1.8) in the active group was significantly (P <0.05, analysis of variance [ANOVA]) better. Similarly, the improvement in the WOMAC scores at week 16 and week 32 were also significantly superior (P <0.01, ANOVA) in the active group. 2) Safety: Both the groups reported mild adverse events (AE) without any significant difference. 3) Withdrawals: Twenty-eight patients were discontinued. None reported drug-related toxicity. The majority failed follow up/compliance. No differences were observed between the groups. CONCLUSION:: This controlled drug trial demonstrates the potential efficacy and safety of RA- 11 in the symptomatic treatment of OA knees over 32 weeks of therapy.
1: Schweiz Arch Tierheilkd. 2004 Feb;146(2):71-9.Links
Dietary support with Boswellia resin in canine inflammatory joint and spinal disease.Reichling J, Schmökel H, Fitzi J, Bucher S, Saller R.
Institut für Pharmazie und Molekulare Biotechnologie (IPMB), Abteilung Biologie, Ruprecht-Karls-University Heidelberg, Germany. Juergen.Reichling@t-online.de

An open multi-centre veterinary clinical trial, comparing conditions before and after treatment with a herbal dietary supplement consisting of a natural resin extract of Boswellia serrata, was conducted by 10 practicing veterinarians in Switzerland. This traditional plant-based supplement is known for its anti-rheumatic and anti-inflammatory properties. 29 dogs with manifestations of chronic joint and spinal disease were enrolled. Osteoarthritis and degenerative conditions were confirmed radiologically in 25 of 29 cases. The resin extract (BSB108, product of Bogar AG) was administered with the regular food at a dose of 400 mg/10 kg body weight once daily for 6 weeks. Already after two weeks of treatment, an overall efficacy of the dietary supplement was evident in 71% of 24 eligible dogs. A statistically significant reduction of severity and resolution of typical clinical signs in individual animals, such as intermittent lameness, local pain and stiff gait, were reported after 6 weeks. Effects of external factors that aggravate lameness, such as "lameness when moving" and "lameness after a long rest" diminished gradually. In 5 dogs, reversible brief episodes of diarrhea and flatulence occurred, but only once was a relationship to the study preparation suspected. Because quality and stability of the resin extract were ensured, these data suggest that a standardized preparation can be recommended as a herbal dietary supplement providing symptomatic support in canine osteoarthritic disease.
29/5/08 owing to increased constipation I have somewhat reluctantly added back the acidophilus which I think may aid the digestive tract. The bioperine is said to be quite constipating. I am now only taking high dose curcumin, moderate dose boswellia, chinese tea inc gentiana macrophyllae and acidophilus. Bad leg feeling quite bouncy.

Posted: Wed May 28, 2008 8:24 am
by cheerleader
Sorry you were rained out in Mallorca, Alex. bummer.
Glad there was wine and sports to take the mind away :)

Thanks for conducting this curcumin and herbal "experiment" and sharing it with all of us. Really glad to hear your leg is faring better back home. Who knows what is placebo and what is "real"? All that matters is how you are feeling. Keep us posted-

best,
AC

Posted: Thu May 29, 2008 6:24 am
by gibbledygook
I've just realised that one of the herbs in the Chinese tea which was recently prescribed is on the list of herbs NOT to have because it induces Epstein Barr...the herb is achyranthes bidentata.
1: Biomed Environ Sci. 1994 Mar;7(1):50-5.Links
Screening of Epstein-Barr virus early antigen expression inducers from Chinese medicinal herbs and plants.Zeng Y, Zhong JM, Ye SQ, Ni ZY, Miao XQ, Mo YK, Li ZL.
Institute of Virology, Chinese Academy of Preventive Medicine, Beijing.

Ether extracts of 1693 Chinese medicinal herbs and plants from 268 families were studied for the induction of Epstein-Barr viral (EBV) early antigen (EA) expression in the Raji cell line. Fifty-two from 18 families were found to have inducing activity. Twenty-five and seven of them were from Euphorbiaceae and Thymelaeaeeae, respectively. Some of them, such as Croton tiglium, Euphorbia kansui, Daphne genkwa, Wikstroemia chamaedaphne, Wikstroemia indica, Prunus mandshurica Koehne and Achyranthes bidentata are commonly used drugs. The significance of these herbs in the activation of EBV in vivo and their relation to the development of nasopharyngeal carcinoma were discussed.
This is annoying as I printed this sheet out for him. Oh well, at least one can order the gentian from the East West shop. I shall stop the tea and instead order the gentian. :?

ps thanks for your comments cheerleader. With a bit of persistence and experimentation I think we should find some effective herbs. At the moment I'm convinced that high dose curcumin and moderate boswellia are reducing by about half the ongoing inflammation that is my MS but...could just be self-brainwashing!!!

30/5/2008 As I'm not taking the chinese tea until the achyranthes bidentatae is taken out (and I'll ask him to replace with rehmannia) I am going to see what, if any, effect the guggul plus formulation has. The total amount of daily herbs here will be 1,134mg of terminalia arjuna, 756mg of piper longum, 756mg of zingiber officinalis, 756mg of piper nigrum, 756mg of emblica officinalis, 756mg of terminalia chebula, 756mg of terminalia belerica, 756mg of trigonella foenum-graecum, 756mg of curcuma longa and 378mg of commiphora mukul. Hopefully the arthritic finger may react as it was a bit more painful this am.

Posted: Sat May 31, 2008 4:28 pm
by mrhodes40
wowee! Thanks for documenting your incredible experiment Gibbles!
I look forward to your final conclusions as to what is what.
marie

Posted: Mon Jun 02, 2008 6:40 am
by gibbledygook
Thanks Marie!


I'm looking for 3 more herbs to balance out the curcumin and boswellia. On my shortlist is the gentianae macrophyllae, rehmannia preparata and withania somnifera.

Here's some stuff on indian ginseng/ashgawandha/withania somnifera:

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Withanoside IV and its active metabolite, sominone, attenuate Abeta(25-35)-induced neurodegeneration.Kuboyama T, Tohda C, Komatsu K.
Division of Biofunctional Evaluation, Research Center for Ethnomedicine, Institute of Natural Medicine, University of Toyama, Toyama 930-0194, Japan.

At the present, medication of dementia is limited to symptomatic treatments such as the use of cholinesterase inhibitors. To cure dementia completely, that is regaining neuronal function, reconstruction of neuronal networks is necessary. Therefore, we have been exploring antidementia drugs based on reconstructing neuronal networks in the damaged brain and found that withanoside IV (a constituent of Ashwagandha; the root of Withania somnifera) induced neurite outgrowth in cultured rat cortical neurons. Oral administration of withanoside IV (10 micromol/kg/day) significantly improved memory deficits in Abeta(25-35)-injected (25 nmol, i.c.v.) mice and prevented loss of axons, dendrites, and synapses. Sominone, an aglycone of withanoside IV, was identified as the main metabolite after oral administration of withanoside IV. Sominone (1 microM) induced axonal and dendritic regeneration and synaptic reconstruction significantly in cultured rat cortical neurons damaged by 10 microM Abeta(25-35). These data suggest that orally administrated withanoside IV may ameliorate neuronal dysfunction in Alzheimer's disease and that the active principle after metabolism is sominone.

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1: Mol Cancer Ther. 2006 Jun;5(6):1434-45. Links
Withanolides potentiate apoptosis, inhibit invasion, and abolish osteoclastogenesis through suppression of nuclear factor-kappaB (NF-kappaB) activation and NF-kappaB-regulated gene expression.Ichikawa H, Takada Y, Shishodia S, Jayaprakasam B, Nair MG, Aggarwal BB.
Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.

The plant Withania somnifera Dunal (Ashwagandha), also known as Indian ginseng, is widely used in the Ayurvedic system of medicine to treat tumors, inflammation, arthritis, asthma, and hypertension. Chemical investigation of the roots and leaves of this plant has yielded bioactive withanolides. Earlier studies showed that withanolides inhibit cyclooxygenase enzymes, lipid peroxidation, and proliferation of tumor cells. Because several genes that regulate cellular proliferation, carcinogenesis, metastasis, and inflammation are regulated by activation of nuclear factor-kappaB (NF-kappaB), we hypothesized that the activity of withanolides is mediated through modulation of NF-kappaB activation. For this report, we investigated the effect of the withanolide on NF-kappaB and NF-kappaB-regulated gene expression activated by various carcinogens. We found that withanolides suppressed NF-kappaB activation induced by a variety of inflammatory and carcinogenic agents, including tumor necrosis factor (TNF), interleukin-1beta, doxorubicin, and cigarette smoke condensate. Suppression was not cell type specific, as both inducible and constitutive NF-kappaB activation was blocked by withanolides. The suppression occurred through the inhibition of inhibitory subunit of IkappaB alpha kinase activation, IkappaB alpha phosphorylation, IkappaB alpha degradation, p65 phosphorylation, and subsequent p65 nuclear translocation. NF-kappaB-dependent reporter gene expression activated by TNF, TNF receptor (TNFR) 1, TNFR-associated death domain, TNFR-associated factor 2, and IkappaB alpha kinase was also suppressed. Consequently, withanolide suppressed the expression of TNF-induced NF-kappaB-regulated antiapoptotic (inhibitor of apoptosis protein 1, Bfl-1/A1, and FADD-like interleukin-1beta-converting enzyme-inhibitory protein) and metastatic (cyclooxygenase-2 and intercellular adhesion molecule-1) gene products, enhanced the apoptosis induced by TNF and chemotherapeutic agents, and suppressed cellular TNF-induced invasion and receptor activator of NF-kappaB ligand-induced osteoclastogenesis. Overall, our results indicate that withanolides inhibit activation of NF-kappaB and NF-kappaB-regulated gene expression, which may explain the ability of withanolides to enhance apoptosis and inhibit invasion and osteoclastogenesis.
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1: Vascul Pharmacol. 2006 Jun;44(6):406-10. Epub 2006 May 18. Links
Immunomodulatory role of Withania somnifera root powder on experimental induced inflammation: An in vivo and in vitro study.Rasool M, Varalakshmi P.
Department of Biosciences, Vellore Institute of Technology, Deemed University, Vellore-632 014, India. mkr474@rediffmail.com

The aqueous suspension of Withania somnifera root powder was investigated for their in vivo and in vitro immunomodulatory properties. W. somnifera showed potent inhibitory activity towards the complement system, mitogen induced lymphocyte proliferation and delayed-type hypersensitivity reaction. Administration of W. somnifera root powder did not have a significant effect on humoral immune response in rats. Our results report immunosuppressive effect of W. somnifera root powder, thus it could be a candidate for developing as an immunosuppressive drug for the inflammatory diseases.
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1: Neurosignals. 2005;14(1-2):34-45. Links
Search for natural products related to regeneration of the neuronal network.Tohda C, Kuboyama T, Komatsu K.
Research Center for Ethnomedicines, Institute of Natural Medicine, Toyama Medical and Pharmaceutical University, Sugitani, Japan.

The reconstruction of neuronal networks in the damaged brain is necessary for the therapeutic treatment of neurodegenerative diseases. We have screened the neurite outgrowth activity of herbal drugs, and identified several active constituents. In each compound, neurite outgrowth activity was investigated under amyloid-beta-induced neuritic atrophy. Most of the compounds with neurite regenerative activity also demonstrated memory improvement activity in Alzheimer's disease-model mice. Protopanaxadiol-type saponins in Ginseng drugs and their metabolite, M1 (20-O-beta-D-glucopyranosyl-(20S)-protopanaxadiol), showed potent regeneration activity for axons and synapses, and amelioration of memory impairment. Withanolide derivatives (withanolide A, withanoside IV, and withanoside VI) isolated from the Indian herbal drug Ashwagandha, also showed neurite extension in normal and damaged cortical neurons. Trigonelline, a constituent of coffee beans, demonstrated the regeneration of dendrites and axons, in addition to memory improvement. 2005 S. Karger AG, Basel
Today (2/6/08) I added back selenium and 2.4g of N acetyl cysteine to my regimen. I don't think I will notice a difference but they are meant to be important for people with MS. Since reintroducing acidophilus the constipation has improved somewhat. I think my bladder is getting a bit stronger and both legs feel firmer and stronger. I continue to be able to lift my bad leg up onto my good leg to put a shoe on and I continue to flex slightly the toe to ease entry of the foot. The morning shower continues to be relatively spasticity free as well so that, unlike before, when the water makes contact with my body, my right leg and arm muscles don't go rigid. My arthritic right index finger had only the slightest pain this morning. ON the downside yesterday I had quite a few phosphenes whilst reading. And I have started sneezing with hayfever which may well be because I have stopped the chinese tea. I do still have a supply of ganoderma lucidum and licorice which were constituents of the previous tea so I may reintroduce them. At least the hayfever is nothing like as bad as it was last year.

3/6/2008
I awoke this morning and for the first time in a few months there was NO pain in my arthritic finger. I think the guggul plus formulation has helped clear things up there although my finger had improved before even starting the guggul plus. As like as not the boswellia and curcumin are also helping. On the down side last night I developed such a blocked eustachian tube that my hearing was affected. Initially I thought I was having an MS attack as the TV started sounding weird but then when I spoke everything sounded even weirder and I realised I couldn't clear the left nose/throat/ear links and that the eustachian was blocked. Hayfever.
Today I will add back some daily zinc and 2000 int units of vit d and some calcium and magnesium supplements. Like the NAC and selenium I don't expect that they will make a noticeable difference but think that they are generally good for people with MS.

A few days ago I mentioned that I thought the high dose curcumin and boswellia had reduced my inflammation by about half. In fact I think they have reduced the inflammation by more than that, conservatively a 75% reduction in inflammation (stiffness, pain, tingling, difficulty walking even bladder functioning much more strongly with less urgency and hesitancy.) Good. For just a month's worth of trial am feeling significantly better and I'd like to think I haven't duped myself on these improvements. When it stops raining in London I shall try to walk a distance without aid and see how far I get. I don't think one can easily fool oneself with walking distance.

For the last month my fingernails have become much tougher. So much so that I can now grow them and file them without them then tearing or splitting. I don't think that in 37 years my fingernails have ever been this tough. Curious. It's not as though I've been taking regular calcium/mag supplements this last month. Also the monthly spots seem much less like boils and more like small pimples.

Posted: Mon Jun 02, 2008 8:20 am
by DIM
What about Polygalae someone mentioned in a different thread?

Posted: Mon Jun 02, 2008 10:09 am
by gibbledygook
Yes, the polygala caudata sounds interesting too. I'll ask my chinese quack... :lol:

Posted: Wed Jun 04, 2008 7:23 am
by gibbledygook
The withania somnifera, Indian ginseng, arrived today and I have already noticed a difference after having taken 4 x 125mg of the life extension pills. My right foot feels a whole lot spongier and different to yesterday. I was intending to take 8 pills a day but I may moderate this as I really think I've already noticed a difference.

I'm still waiting for the rehmannia and gentianae macrophyllae to arrive in the post but hopefully my chinese doctor will order these for me when I see him at the end of the month. I continue with the curcumin, boswellia, the guggul plus formulation, NAC, selenium, zinc, vit d, mag & calcium.

I was going to PM Schnittke to answer his question about whether or not I think the life extension curcumin tabs are better than others when I realised I hadn't yet tested anything very much empirically. I decided to go on a walk on a sunny warm London afternoon and this is the result: I managed 650 meters unaided and the next 250 with the cane, I rested for half an hour and then foolishly attempted to walk back and needed the cane for most of the 900 meters and then failed to make it home in time for the toilet! This is what comes of over-optimism. However considering that during my February relapse I could barely manage 5 meters I have been improving, slowly and irregularly. On 12 April 08 and somewhat hungover I can just about manage 150 meters with a cane. Around the 22nd April I manage around 400 meters with a cane on uneven ground. On May 1 I manage 800 meters with a cane. On May 13 I manage 500 meters unaided and the next 200 meters on an arm. So I have been improving and I THINK that the Life Extension bio curcumin is better than the stuff I was using before but of course it could be random. Mind you, the curcumin of whatever flavour is the only med that I have consistently taken in relatively high dose since my relapse at the end of February so there is a chronological convergence between curcumin consumption and walking improvement.

Posted: Thu Jun 05, 2008 1:43 am
by gibbledygook
more herbal ideas:
1: Arthritis Res Ther. 2007;9(4):R70. Links
Celastrus aculeatus Merr. suppresses the induction and progression of autoimmune arthritis by modulating immune response to heat-shock protein 65.Tong L, Moudgil KD.
Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Complementary and alternative medicine products are increasingly being used for the treatment of autoimmune diseases. However, the mechanisms of action of these agents are not fully defined. Using the rat adjuvant arthritis (AA) model of human rheumatoid arthritis, we determined whether the ethanol extract of Celastrus aculeatus Merr. (Celastrus), a Chinese herb, can down-modulate the severity of AA, and also examined the Celastrus-induced changes in immune responses to the disease-related antigen mycobacterial heat-shock protein 65 (Bhsp65). AA was induced in the Lewis (LEW; RT.1l) rat by immunization subcutaneously with heat-killed M. tuberculosis H37Ra (Mtb). Celastrus was fed to LEW rats by gavage daily, beginning either before Mtb challenge (preventive regimen) or after the onset of AA (therapeutic regimen). An additional group of rats was given methotrexate for comparison. All rats were graded regularly for the signs of arthritis. In parallel, the draining lymph node cells of Celastrus-treated rats were tested for proliferative and cytokine responses, whereas their sera were tested for the inflammatory mediator nitric oxide. Celastrus feeding suppressed both the induction as well as the progression of AA, and the latter effect was comparable to that of methotrexate. Celastrus treatment induced relative deviation of the cytokine response to anti-inflammatory type and enhanced the production of anti-Bhsp65 antibodies, which are known to be protective against AA. Celastrus feeding also reduced the levels of nitric oxide. On the basis of our results, we suggest further systematic exploration of Celastrus as an adjunct therapeutic modality for rheumatoid arthritis.
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1: J Pharmacol Sci. 2006 Jan;100(1):41-50. Epub 2006 Jan 11. Links
Anti-arthritic effects of Ephedra sinica STAPF herb-acupuncture: inhibition of lipopolysaccharide-induced inflammation and adjuvant-induced polyarthritis.Yeom MJ, Lee HC, Kim GH, Lee HJ, Shim I, Oh SK, Kang SK, Hahm DH.
Laboratory of Acupuncture & Meridian, Department of Oriental Medical Science, Graduate School of East-West Medical Science, Kyung-Hee University, Kyungki-do, Korea.

Anti-inflammatory and anti-arthritic effects of water distillates of Ephedra sinica STAPF (ES), in herb-acupuncture, on the inflammatory responses of arthritis was investigated using phorbol 12-myristate 13-acetate (PMA)/lipopolysaccharide (LPS)-induced human macrophage and adjuvant-induced arthritic rat. The luciferase reporter vectors driven by the tumor necrosis factor (TNF)-alpha and cyclooxygenase-2 promoters were transiently transfected into U937 cells, which were then differentiated and stimulated by PMA and LPS, respectively, to develop an in vitro anti-inflammation assay system. The luciferase activities, observed in the activated U937 cells, were significantly inhibited by ES herb-acupuncture, compared to those of PD98509 and berberine. To evaluate ES herb-acupuncture as a novel anti-arthritic therapy, a polyarthritic rat model was developed using heat-killed Mycobacterium tuberculosis, and 50 mul of ES distillate was subcutaneously injected into the ST36 acupoint on each knee joint. While the articular indexes of arthritic rats were evidently decreased by ES herb-acupuncture, their body weights did not regain their initial levels. This may be due to the accelerating effects of ES on weight-loss and fat consumption. The mRNA expressions of TNF-alpha and interleukin (IL)-6 genes, which were closely stimulated in the arthritic rat joints, were found to be restored to the normal levels through the ES treatment. In the case of IL-1beta, the recovery was not significant but substantial. The anti-arthritic effect of ES herb-acupuncture was not found in the ES-treated/non-acupoint group. In conclusion, the ES herb-acupuncture into the ST36 acupoint was found to be effective in alleviating the inflammatory response and thus arthritic symptoms in adjuvant-induced arthritic rats.
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1: Zhongguo Zhong Yao Za Zhi. 2004 Jun;29(6):542-5.Links
[Experimental research of effect of crude and processed Herba Siegesbeckiae on anti-inflammation and anti-rheumatism][Article in Chinese]


Hu HH, Tang LX, Li XM.
College of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100102, China. shuihh@263.net

OBJECTIVE: To find out the specialities of the effect of crude and processed Herba Siegesbeckiae on anti-inflammation and anti-rheumatism. METHOD: Experiments were made on rats with swelling foot induced by carrageenin; experiments were made on mice with swelling ear induced by xylol; experiments were made on rats with chronic granuloma; experiments were made on rats with adjuvant arthritis. RESULT: Foot swelling induced by carrageenin could be diminished with crude and processed Herba Siegesbeckiae at 6.0, 2.0 g x kg(-1). The rate of inhibition of foot swelling was more than 40%, effect of the crude drug was better than that of the processed one; both of them at 6.0, 2.0 g x kg(-1) could protect rats from primary and continuous lesion of adjuvant arthritis. The effect of the processed herb was obviously better than that of the crude one in its starting minute, strength and sustaining time. CONCLUSION: The processed Herba Siegesbeckiae has obvious inhibition effect on immune inflammation. It is better than the crude Herb. Both of them have obvious inhibition effect on inflammation caused by carrageenin, with no distinct difference.
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1: Br J Pharmacol. 2004 Dec;143(7):919-27. Epub 2004 Oct 25. Links
Plant alkaloid tetrandrine downregulates IkappaBalpha kinases-IkappaBalpha-NF-kappaB signaling pathway in human peripheral blood T cell.Ho LJ, Juan TY, Chao P, Wu WL, Chang DM, Chang SY, Lai JH.
Division of Gerontology Research, National Health Research Institute, Taipei, Taiwan, ROC.

Plant alkaloid tetrandrine (Tet), purified from Chinese herb Han-Fang Chi, is a potent immunomodulator used to treat rheumatic disorders, silicosis and hypertension in mainland China. We previously demonstrated that Tet effectively suppresses cytokine production and proliferation of CD28-costimulated T cells. In the present study, we investigated the possible involvement of nuclear factor kappa B (NF-kappaB) transcription factors, critical in CD28 costimulation, in Tet-mediated immunosuppression in human peripheral blood T cells. We showed that Tet inhibited NF-kappaB DNA-binding activities induced by various stimuli, including CD28 costimulation. At equal molar concentrations, Tet was as strong as methotrexate in suppressing CD28-costimulated NF-kappaB activities. Since Tet itself did not affect NF-kappaB binding to its corresponding DNA sequence, the results suggested that Tet might regulate NF-kappaB upstream signaling molecules. Further studies demonstrated that Tet could prevent the degradation of IkappaBalpha and inhibit nuclear translocation of p65 by blocking IkappaBalpha kinases alpha and beta activities. In addition, the activation of mitogen-activated protein kinases such as c-jun N-terminal kinase, p38 and extracellular signal-regulated kinase and activator protein-1 DNA-binding activity were all downregulated by Tet. Transfection assays performed in purified human peripheral blood T cells also confirmed the inhibition of NF-kappaB transcriptional activity by Tet. When four Tet analogues were readily compared, dauricine appeared to preserve the most potent inhibition on CD28-costimulated but not on H(2)O(2)-induced NF-kappaB DNA-binding activities. Our results provide the molecular basis of immunomodulation of Tet for being a potential disease-modifying antirheumatic drug in the therapy of autoimmune disorders like rheumatoid arthritis.
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Unfortunately tripterygium wilfordi. is very toxic, and my chinese quack won't prescribe it. The tet can also be toxic in doses of over 30g and intravenously it can be toxic indoses of greater than 240mg.
1: Curr Drug Metab. 2004 Apr;5(2):181-92. Links
Chinese herbs as immunomodulators and potential disease-modifying antirheumatic drugs in autoimmune disorders.Ho LJ, Lai JH.
Division of Gerontology Research, National Health Research Institute,Taipei, Taiwan, ROC. haungben@tpts5.seed.net.tw

Autoimmune diseases are a group of illnesses with multiple organ involvement. The prototype of this group of disorders is rheumatoid arthritis (RA) that aside from systemic organ involvement mainly presents with progressive destruction of many joints. Both activation and defective apoptosis of immune effector cells like T and B lymphocytes and macrophages play critical roles in the pathogenesis of autoimmune disorders. Current therapy for autoimmune diseases recommends a combination of several disease-modifying antirheumatic drugs (DMARDs) that preserve different immunomodulatory mechanisms. Because of limited success in prevention of RA joint destruction for currently available DMARDs, the development of more effective and less toxic DMARDs has been one of the major goals for pharmaceutical companies. The introduction of leflunomide and anti-tumor necrosis factor alpha therapies to the market recently serves as examples. In this context, the experience from ancient Chinese medicine gives an alternative consideration looking for potential DMARDs. Two commonly prescribed Chinese antirheumatic herbs are Tripterygium wilfordii hook f (TWHf) and tetrandrine (Tet) that preserve both anti-inflammatory and immunosuppressive effects. Importantly, the TWHf- or Tet-mediated immunomodulatory mechanisms are evidently different from the known DMARDs. The synergistic effects have also been demonstrated between these two Chinese antirheumatic herbs and DMARDs like FK506, cyclosporin and possibly chloroquine. Another potential Chinese herb for this consideration is Ginkgo biloba. This review summarizes evidence-based in vivo and in vitro studies on Chinese herbs as immunomodulators and potential DMARDs.
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1: Drugs R D. 2003;4(1):1-18.Links
Immunosuppressive and anti-inflammatory mechanisms of triptolide, the principal active diterpenoid from the Chinese medicinal herb Tripterygium wilfordii Hook. f.Qiu D, Kao PN.
Division of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, California 94305, USA. peterkao@stanford.edu

Extracts of Tripterygium wilfordii hook. f. (leigong teng, Thundergod vine) are effective in traditional Chinese medicine for treatment of immune inflammatory diseases including rheumatoid arthritis, systemic lupus erythematosus, nephritis and asthma. Characterisation of the terpenoids present in extracts of Tripterygium identified triptolide, a diterpenoid triepoxide, as responsible for most of the immunosuppressive, anti-inflammatory and antiproliferative effects observed in vitro. Triptolide inhibits lymphocyte activation and T-cell expression of interleukin-2 at the level of transcription. In all cell types examined, triptolide inhibits nuclear factor-kappaB transcriptional activation at a unique step in the nucleus after binding to DNA. Further characterisation of the molecular mechanisms of triptolide action will serve to elucidate pathways of immune system regulation.
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1: Acta Pharmacol Sin. 2002 Dec;23(12):1093-101.Links
Immunomodulatory effects and mechanisms of plant alkaloid tetrandrine in autoimmune diseases.Lai JH.
Rheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, China. haungben@tpts5.seed.net.tw

Autoimmune diseases characterized by activation of immune effector cells and damage of target organs are currently treated with a combination of several disease-modifying antirheumatic drugs (DMARDs) that preserve different immunomodulatory mechanisms. Such a combination treatment strategy not only provides synergistic effects but also reduces side effects from individual drug. Tetrandrine (Tet), purified from a creeper Stephania tetrandra S Moore, is a bis-benzylisoquinoline alkaloid and has been used to treat patients with silicosis, autoimmune disorders, and hypertension in Mainland China for decades. The accumulated studies both in vitro and in vivo reveal that Tet preserves a wide variety of immunosuppressive effects. Importantly, the Tet-mediated immunosuppressive mechanisms are evidently different from some known DMARDs. The synergistic effects have also been demonstrated between Tet and other DMARDs like FK506 and cyclosporin. These results highlight Tet a very potential candidate to be considered as one of DMARDs in the treatment of autoimmune diseases, especially rheumatoid arthritis. This review summarizes evidence-based in vivo and in vitro studies on this potential Chinese immunosuppressive herb
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1: Mediators Inflamm. 1996;5(4):280-91. Links
Anti-inflammatory effects of Stephania tetrandra S. Moore on interleukin-6 production and experimental inflammatory disease models.Kang HS, Kim YH, Lee CS, Lee JJ, Choi I, Pyun KH.
Immune Cell Signal Transduction R.U. Korea Research Institute of Bioscience and Biotechnology KIST Yusong, P.O. Box 115 Taejon 305-600 Korea.

Deregulation of interleukin-6 (IL-6) expression caused the synthesis and release of many inflammatory mediators. It is involved in chronic inflammation, autoimmune diseases, and malignancy. Stephania tetrandra S. Moore is a Chinese medicinal herb which has been used traditionary as a remedy for neuralgia and arthritis in China. To investigate the anti-inflammatory effects of S. tetrandra S. Moore in vitro and in vivo, its effects on the production of IL-6 and inflammatory mediators were analysed. When human monocytes/macrophages stimulated with silica were treated with 0.1-10 mug/ml S. tetranda S. Moore, the production of IL-6 was inhibited up to 50%. At these concentrations, it had no cytotoxicity effect on these cells. It also suppressed the production of IL-6 by alveolar macrophages stimulated with silica. In addition, it inhibited the release of superoxide anion and hydrogen peroxide from human monocytes/macrophages. To assess the anti-fibrosis effects of S. tetrandra S. Moore, its effects on in vivo experimental inflammatory models were evaluated. In the experimental silicosis model, IL-6 activities in the sera and in the culture supernatants of pulmonary fibroblasts were also inhibited by it. In vitro and in vivo treatment of S. tetrandra S. Moore reduced collagen production by rat lung fibroblasts and lung tissue. Also, S. tetrandra S. Moore reduced the levels of serum GOT and GPT in the rat cirrhosis model induced by CCL(4), and it was effective in reducing hepatic fibrosis and nodular formation. Taken together, these data indicate that it has a potent anti-inflammatory and antifibrosis effect by reducing IL-6 production.
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1: Biol Pharm Bull. 2007 Aug;30(8):1438-44. Links
Sinomenine, an antirheumatic alkaloid, ameliorates clinical signs of disease in the Lewis rat model of acute experimental autoimmune encephalolmyelitis.Zeng Y, Gu B, Ji X, Ding X, Song C, Wu F.
Department of Immunology, Nanjing Medical University, 140 Hanzhong Road, Nanjing 210029, China.

The therapeutic value of an antirheumatic alkaloid, sinomenine (SIN), was investigated in the acute experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). SIN is a bioactive alkaloid derived from the Chinese medicinal plant, Sinomenium acutum REHDER & E. H. WILSON (Family Menispermaceae). Chinese doctors have utilized this plant to treat rheumatic and arthritic diseases for over one thousand years. Experiments in which EAE-induced Lewis rats exhibit an acute monophasic episode of disease demonstrated that SIN is effective in preventing clinical signs of disease. The therapeutic effect on disease activity was observed at preonset administration times and at various doses tested. Consistent with disease activity in vivo, SIN-treated animals have reduced cellular infiltration within the spinal cord along with decreased TNF-alpha and IFN-gamma expression levels. SIN can significantly inhibit proliferation response of splenocytes induced by MBP(68-82). TNF-alpha and IFN-gamma, secreted by splenocytes induced by MBP(68-82) are inhibited by SIN by dose-dependence manner. The mRNA levels of CC chemokines, RANTES, MIP-1alpha and MCP-1, are inhibited in SIN-treated EAE rats. The data in this proof of concept study support the premise that SIN may be a promising new therapeutic intervention in MS.
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1: J Neurosci Res. 2007 Apr;85(5):954-66. Links
Restoration of FcRgamma/Fyn signaling repairs central nervous system demyelination.Seiwa C, Yamamoto M, Tanaka K, Fukutake M, Ueki T, Takeda S, Sakai R, Ishige A, Watanabe K, Akita M, Yagi T, Tanaka K, Asou H.
Department of Neuro-Glia Cell Biology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.

Disruption of myelin causes severe neurological diseases. An understanding of the mechanisms that control myelination and remyelination is needed to develop therapeutic strategies for demyelinating diseases such as multiple sclerosis (MS). Our previous finding indicating the critical involvement of the gamma chain of immunogloblin Fc receptors (FcRgamma) and Fyn signaling in oligodendrocyte differentiaion and myelination demands a fundamental revision of the strategies used for MS therapy, because antigen-antibody complexes in MS patients may induce the direct dysregulation of myelination process as well as the inflammatory destruction of myelin sheath. Here we show that the FcRgamma/Fyn signaling cascade is critically involved in cuprizone-induced demyelination/remyelination, with no lymphocytic response. The levels of phosphorylated myelin basic proteins (p-MBPs), especially the 21.5-kDa isoform, but not the levels of total MBPs, decreased markedly during demyelination induced by aging, cuprizone treatment, and double knockout of FcRgamma/Fyn genes. We also showed that the recovery from demyelination in cuprizone-treated and aged mice is achieved after administration of the herbal medicine Ninjin'yoeito, an effective therapy targeting the FcRgamma/Fyn-Rho (Rac1)-MAPK (P38 MAPK)-p-MBPs signaling cascade. These results suggest that the restoration of FcRgamma/Fyn signaling represents a new approach for the treatment of demyelinating diseases. (c) 2007 Wiley-Liss, Inc.
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What is that then?
Titre du document / Document title
Therapeutic effect of a traditional Chinese medicine, ren-shen-yang-rong-tang (Japanese name: Ninjin'yoeito) on nitric oxide-mediated lung injury in a mouse infected with murine cytomegalovirus
Auteur(s) / Author(s)
TANAKA Kazuo (1) ; SAWAMURA Sadaaki (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Laboratory of Infections Diseases, Tokai University School of Medicine, Bohseidai, Isehara, Kanagawa 259-1193, JAPON

Résumé / Abstract
The therapeutic effect of a traditional Chinese medicine ren-shen-yang-rong-tang (Japanese name: Ninjin'yoeito, NYT) on murine cytomegalovirus (MCMV)-associated pneumonitis was examined. In MCMV-pneumonitis, IFN-γ-induced nitric oxide (NO) mediates its pathogenesis. When mice, which had been infected with 0.2LD50 of MCMV at 28 days previously, were intraperitoneally injected with anti-CD3 monoclonal antibody (mAb), MCMV-pneumonitis was induced in the lung, where high amounts of IFN-γ-producing cells thereafter accumulated, accompanied by an elevation in the NO level in the serum and abundant expression of inducible NO synthase (iNOS) mRNA, thus resulting in all mice eventually dying. When the mice were orally treated with NYT (1000 mg/kg/day) once on the day of mAb injection and once the day after, the expression level of iNOS-mRNA was suppressed and NO level in the serum decreased. The survival rate improved from 0% to 57.1%. The pathological findings of the lungs in the NYT-treated mice were comparable to those of the uninfected controls. In contrast, NYT itself did not affect either the ratio of IFN-γ-producing cells or MCMV titer. As a result, NYT had a therapeutic effect on MCMV-pneumonitis by decreasing the degree of inflammation mediated by the IFN-γ-induced NO. It is also interesting to note that only two oral administrations of NYT had a therapeutic effect on viral disease.
Revue / Journal Title
International immunopharmacology ISSN 1567-5769
http://cat.inist.fr/?aModele=afficheN&cpsidt=17569319

What is ren shen yang rong tang?
ren shen yang rong tang 人 參 養 榮 湯

Edited and translated by: Joe Hing Kwok Chu

Name of Formula: ren shen yang rong tang (source: He Ju Ji Fang)

Application: for qixu and blood deficiency

Formula:

bai shao 18 g, dang gui 15 g, chen pi 12 g, huang qi 30 g, rou gui 6 g, ren shen 15 g (boil first), bai zhu 15 g, zhi gan cao 9 g, shu di 15 g, wu wei zi 12 g, fu ling 15 g, yuan zhi 9 g, he shou wu 30 g, dan shen 30 g, ji xue teng 30 g, sheng jiang 6 g, da zao 7 pieces. Add 1000 c.c. of water. Simmer till 200 ~ 300 c.c. Make into 2 serving. Drink while warm
http://alternativehealing.org/ren_shen_ ... g_tang.htm
The translation is in the same order, paeoniae radix, angelica sinensis, citri reticulatae pericarpium, astragali radix, cinnamoni cortex, ginseng radix,, astractylodis macrocephelae rhizoma, maybe ganoderma and glycyrrhizae radix, rehmannia radix preparata, shisandra fructus, poria, polygalae radix, polygoni multiflori radix preparata, salviae miltiorrhizae radix, spatholobi caaulis, drynorae rhizoma, jujubae fructus. Phewee, probably best to try the formula rather than the individual herbs!

More good news on this formulation:
Effect of a traditional Chinese herbal medicine, Ren-Shen-Yang-Rong-Tang (Japanese name: Ninjin-Youei-To), on oligodendrocyte precursor cells from aged-rat brain

Junko Kobayashia, b, Chika Seiwaa, Tomomi Sakaia, Mari Gotoha, Yasuhiro Komatsua, c, Masahiro Yamamotoa, d, Masato Fukutakea, d, Kenjiro Matsunoe, Yoko Sakuraia, Yukari Kawanob and Hiroaki Asoua, ,

a Department of Neuro-cell Biology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakaecho, Itabashi, Tokyo 173-0015, Japan

b Graduate School of Sports Nutrition, Japan Women's College of Physical Education, 8-19-1 Kitakarasuyama, Setagaya, Tokyo 157-8565, Japan

c Department of Serology, Kanazawa Medical School, Uchinadamachi 920-0293, Japan

d Kampo Pharmacology Department, Tsumura Central Research Laboratories, Tsumura & Co., Ibaraki 300-1192, Japan

e Department of Anatomy II, Kumamoto University, School of Medicine, Kumamoto 860-0811, Japan


Accepted 9 April 2003. ; Available online 13 May 2003.




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Abstract
Understanding of oligodendrocyte precursor cells and their role in the generation of oligodendrocytes in developing and adult rodents has been considered, particularly much less is known about aged-rodent oligodendrocyte precursor cells and their cell lineage. In this present study, we have developed oligodendrocyte cultures from the 30-month-old rat brain and examined whether oligodendrocyte precursor cells can proliferate in vitro. Adult oligodendrocyte precursor cells (O1−, O4+) and oligodendrocytes (O1+, O4+) are present in the cultures of the 30-month-old rat brain. They are also capable of proliferating and differentiating in the cultures. These capabilities increased four- to fivefold, when the aged rats are treated with Ninjin-Youei-To for 3 months in comparison with those of control aged rats. These results suggest that Ninjin-Youei-To has a potential mitotic effect on oligodendrocyte precursor cells in aged-rat brains and may be expected to have a therapeutic effect on brain aging.
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Posted: Thu Jun 05, 2008 3:37 am
by DIM