I am now in full cold/flu mode with sore throat and odd temperature changes and sneezing fits. Curiously the dose of ginkgo/salvia that seemed pretty good yesterday is producing somewhat greater stiffness today. The dose yesterday was 240mg ginkgo with 1020mg salvia every 3 to 3.5 hours and 7 times in all. This works out at 1.68g of ginkgo and 7.140g of salvia. I had a few spasms at night and think I shall increase to 3 ginkgo this evening. Perhaps this increase in stiffness is owing to the effects of infection on the endothelium:
1: Atherosclerosis. 2005 Feb;178(2):345-50. Links
Acute inflammatory state during influenza infection and endothelial function.Marchesi S, Lupattelli G, Lombardini R, Sensini A, Siepi D, Mannarino M, Vaudo G, Mannarino E.
Internal Medicine Section, Department of Clinical and Experimental Medicine, University of Perugia, Italy.
simonamarchesi@yahoo.it
Chronic inflammatory stimulus seems to contribute to atherosclerotic process. Several studies have established a relationship between infective agents as Chlamydia pneumoniae, herpes virus and cytomegalovirus and atherosclerotic lesions. Aim of this study was to investigate the effects of influenza infective state on endothelial function of healthy young subjects, expressed as brachial flow-mediated vasodilation (FMV) and soluble form of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1). In 10 male subjects (mean age 35+/-14 years) exhibiting influenza symptoms for 3 days, we determined total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), triglycerides, sVCAM-1, sICAM-1 and brachial FMV. All subjects had an antibody pattern characteristic of influenza A or B virus infection.
After 3 months brachial FMV was significantly increased (8.6+/-2.3% versus 11.5+/-3.2%; p<0.001), while HDL (46+/-10 mg/dL versus 49+/-9 mg/dL; p<0.05),
sICAM-1 and sVCAM-1 were reduced (respectively: 488+/-105 ng/mL versus 340+/-127 ng/mL; p<0.001, 1710+/-80 ng/mL versus 1216+/-63 ng/mL; p<0.001). Univariate analysis showed a positive correlation between changes in CRP and sICAM-1 levels (r=0.95, p<0.001), a negative one between changes in sICAM-1 and brachial FMV (r=-0.65, p<0.05) and between CRP and brachial FMV (r=-0.64, p<0.05). This small study suggested that
inflammatory state determined by viral agents may transitorily alter endothelial function in healthy subjects.
PMID: 15694944 [PubMed - indexed for MEDLINE]
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1: Thromb Haemost. 2000 Aug;84(2):319-24. Links
Procoagulant activity of endothelial cells after infection with respiratory viruses.Visseren FL, Bouwman JJ, Bouter KP, Diepersloot RJ, de Groot PH, Erkelens DW.
Department of Internal and Vascular Medicine, University Medical Center Utrecht, The Netherlands.
F.Visseren@digd.azu.nl
Influenza virus epidemics are associated with excess mortality due to cardiovascular diseases. There are several case reports of excessive coagulation during generalised influenza virus infection. In this study, we demonstrate the ability of respiratory viruses (influenza A, influenza B, parainfluenza-1, respiratory syncytial virus, adenovirus, cytomegalovirus) to infect lung fibroblasts and human umbilical vein endothelial cells in culture. All viral pathogens induced procoagulant activity in infected endothelial cells, as determined in a one-stage clotting assay, by causing an average 55% reduction in the clotting time. When factor VII deficient plasma was used clotting time was not reduced.
The induction of procoagulant activity was associated with a 4- to 5-fold increase in the expression of tissue factor, as measured by the generation of factor Xa. Both experiments indicate that the procoagulant activity of endothelial cells in response to infection with respiratory viruses is caused by upregulation of the extrinsic pathway. Although both enveloped viruses and a non-enveloped virus (adenovirus) induced procoagulant activity in endothelial cells by stimulating tissue factor expression, the role of the viral envelope in the assembly of the prothrombinase complex remains uncertain. We conclude that both enveloped and non-enveloped respiratory viruses are capable of infecting cultured human endothelial cells and causing a shift from anticoagulant to procoagulant activity associated with the induction of tissue factor expression.
PMID: 10959707 [PubMed - indexed for MEDLINE]
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Therefore need some artemisia scoporia which I can't find exactly at herbalextractsplus (just using them for reference) but can find lots of artemisia:
1: J Biomed Sci. 2003 Sep-Oct;10(5):518-25.Links
Scoparone inhibits tissue factor expression in lipopolysaccharide-activated human umbilical vein endothelial cells.Lee YM, Hsiao G, Chang JW, Sheu JR, Yen MH.
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, ROC.
ymlee@ndmctgh.edu.tw
Tissue factor (TF) is an important regulator and effector molecule of coagulation in various inflammatory states. In sepsis, expression of TF by activated endothelial cells leads to disseminated intravascular coagulation. Scoparone is extracted from the traditional Chinese herb ARTEMISIA SCOPARIA and is known to have potent anti-inflammatory properties. In the current studies, we examined the effects of scoparone on inhibiting lipopolysaccharide (LPS)-induced TF expression in cultured human umbilical vein endothelial cells (HUVECs).
Flow-cytometric analysis revealed LPS (10 micro g/ml)-activated surface TF induction was concentration-dependently inhibited by scoparone (10-400 micro M). The concentrations of scoparone used in this study did not affect cell viability. The elevation of the procoagulant activity of TF by LPS was suppressed by scoparone. The LPS-induced superoxide formation was markedly decreased by scoparone. Messenger RNA expression of TF in LPS-activated HUVECs was also reduced by scoparone. Furthermore, scoparone did not significantly affect the IkappaBalpha degradation. Our results demonstrate that the inhibition of scoparone on LPS-induced TF expression in HUVECs may mediate by the mechanisms suppressing superoxide anion formation and TF transcription. Copyright 2003 National Science Council, ROC and S. Karger AG, Basel
PMID: 12928592 [PubMed - indexed for MEDLINE]
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from herbalextractsplus
Botanical: Artemisia vulgaris
Family: Compositae (daisy) - Asteraceae (aster)
Other common names: Felon Herb, Cingulum Sancti Johannis, Saint John's Plant,
Common Artemisia, Wild Wormwood, Chinese Moxa, Sailor's Tobacco
or
Botanical: Artemisia absinthium
Family: Compositae (daisy)
Other common names: Absinthe, Green Ginger, Absinthium, Old Woman, Southernwood, Wormwood, Wermutkraut, Southern Wood
Now I actually have a small pot of this so I shall give it a whirl.
or jiaogulan:
1: Toxicol Appl Pharmacol. 2007 Jan 1;218(1):30-6. Epub 2006 Oct 25. Links
Gypenoside XLIX, a naturally occurring gynosaponin, PPAR-alpha dependently inhibits LPS-induced tissue factor expression and activity in human THP-1 monocytic cells.Huang TH, Tran VH, Roufogalis BD, Li Y.
Faculty of Pharmacy, University of Sydney, NSW 2006, Australia.
Tissue factor (TF) is involved not only in the progression of atherosclerosis and other cardiovascular diseases, but is also associated with tumor growth, metastasis, and angiogenesis and hence may be an attractive target for directed cancer therapeutics. Gynostemma pentaphyllum (GP) is widely used in the treatment of various cardiovascular diseases including atherosclerosis, as well as cancers. Gypenoside (Gyp) XLIX, a dammarane-type glycoside, is one of the prominent components in GP. We have recently reported Gyp XLIX to be a potent peroxisome proliferator-activated receptor (PPAR)-alpha activator. Here we demonstrate that Gyp XLIX (0-300 microM) concentration dependently inhibited TF promoter activity after induction by the inflammatory stimulus lipopolysaccharide (LPS) in human monocytic THP-1 cells transfected with promoter reporter constructs pTF-LUC. Furthermore, Gyp XLIX inhibited LPS-induced TF mRNA and protein overexpression in THP-1 monocyte cells. Its inhibition of LPS-induced TF hyperactivity was further confirmed by chromogenic enzyme activity assay. The activities of Gyp XLIX reported in this study were similar to those of Wy-14643, a potent synthetic PPAR-alpha activator. Furthermore, the Gyp XLIX-induced inhibitory effect on TF luciferase activity was completely abolished in the presence of the PPAR-alpha selective antagonist MK-886. The present findings suggest that Gyp XLIX inhibits LPS-induced TF overexpression and enhancement of its activity in human THP-1 monocytic cells via PPAR-alpha-dependent pathways. The data provide new insights into the basis of the use of the traditional Chinese herbal medicine G. pentaphyllum for the treatment of cardiovascular and inflammatory diseases, as well as cancers.
PMID: 17141290 [PubMed - indexed for MEDLINE]
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From wikipedia:
Gynostemma pentaphyllum, also called jiaogulan (Chinese: 绞股蓝; pinyin: jiǎogǔlán, literally "twisting-vine-orchid") is an herbaceous vine of the family Cucurbitaceae (cucumber or gourd family) indigenous to the southern reaches of China, southern Korea and Japan. Jiaogulan is best known as an herbal medicine reputed to have powerful antioxidant and adaptogenic effects that increase longevity.
Western languages such as English and German commonly refer to the plant as jiaogulan. Other names include:[7]
Chinese: xiancao (仙草, literally "immortal grass"; more accurately "herb of immortality")
English: five-leaf ginseng, poor man's ginseng, miracle grass, fairy herb, sweet tea vine, gospel herb
from herbalextractsplus which supplies it:
Botanical: Gynostemma pentaphyllum
Family: Cucurbitaceae (gourd/squash)
Other common names: Southern Ginseng, Jiaogulan, Sweet Tea Vine, Gospel Herb,
Amachazuru (Japan), Dungkulcha (Korea)
or kudzu which increases TF activity although I'm not at all certain that this would be good in MS.
1: J Med Food. 2004 Spring;7(1):31-7. Links
Effect of kaikasaponin III obtained from Pueraria thunbergiana flowers on serum and hepatic lipid peroxides and tissue factor activity in the streptozotocin-induced diabetic rat.Choi J, Shin MH, Park KY, Lee KT, Jung HJ, Lee MS, Park HJ.
College of Pharmacy, Kyungsung University, Korea.
We investigated the effect of kaikasaponin III (KS-III) on Phase I and II enzymes and tissue factor (TF) activity to elucidate the pharmacological actions of this immunosuppressive saponin in the diabetic rat. This compound was obtained from the flower of Pueraria thunbergiana (Leguminosae) by chromatographic isolation. This crude drug (Puerariae Flos) has been used as a therapeutic agent for diabetes mellitus in traditional Korean medicine. KS-III prolonged the bleeding time and plasma clotting time in streptozotocin (STZ)-treated rats and increased the TF activity, suggesting that this compound has anti-thrombosis activity in STZ-induced rats. It also inhibited the formation of malondialdehyde (MDA) and hydroxy radicals in serum and liver, but promoted superoxide dismutase (SOD) activity. Low MDA concentrations and low xanthine oxidase and aldehyde oxidase activities were observed in the KS-III-treated rats, suggesting that such Phase I enzyme activities are the major source of lipid peroxidation. However, KS-III increased Phase II enzyme activities such as SOD, glutathione peroxidase, and catalase, suggesting the activation of free radical-scavenging enzymes. These results suggest that KS-III may exhibit its hypoglycemic and hypolipidemic effects by up-regulating or down-regulating antioxidant mechanisms via the changes in Phase I and II enzyme activities.
PMID: 15117550 [PubMed - indexed for MEDLINE]
Related ArticlesHypoglycemic and hypolipidemic effects of tectorigenin and kaikasaponin III in the streptozotocin-lnduced diabetic rat and their antioxidant activity in vitro. [Arch Pharm Res. 2000] Potent antimutagenic and their anti-lipid peroxidative effect of kaikasaponin III and tectorigenin from the flower of Pueraria thunbergiana. [Arch Pharm Res. 2002] Alternation of hepatic antioxidant enzyme activities and lipid profile in streptozotocin-induced diabetic rats by supplementation of dandelion water extract. [Clin Chim Acta. 2002] ReviewEffects of pineal peptide preparation Epithalamin on free-radical processes in humans and animals. [Neuro Endocrinol Lett. 2001] Review[Advances in the studies of saponins from Aralia] [Yao Xue Xue Bao. 1997] » See Reviews... | » See All...
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from herbalextractsplus:
Botanical: Pueraria lobata
Family: Fabaceae (legume)
Other common names: Kuzu, Pueraria, Gwat Gun, Ge Gan, Pueraria Root, Japanese Arrowroot
A staple in Japanese and Chinese herbal medicine, Kudzu has been a traditional treatment for stiff neck, headache, muscle tension and neurological conditions. For over two thousand years, Chinese physicians have relied on it to reduce alcohol abuse, relieve respiratory problems and counteract poisons.
we need some natural iron chelators:
1: Eur J Clin Invest. 2002 Mar;32 Suppl 1:84-90. Links
Iron chelation and hydroxyl radical scavenging reduce the inflammatory response of endothelial cells after infection with Chlamydia pneumoniae or influenza A.Visseren FL, Verkerk MS, van der Bruggen T, Marx JJ, van Asbeck BS, Diepersloot RJ.
Department of Internal and Vascular Medicine, Room F.02.126, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
f.visseren@digd.azu.nl
BACKGROUND: Chronic low-grade inflammation is associated with increased risk of vascular diseases. The source of inflammation is unknown but may well be chronic and/or repetitive infections with microorganisms. Direct infection of endothelial cells (ECs) may also be a starting point for atherogenesis by initiating endothelial procoagulant activity, increased monocyte adherence and increased cytokine production. We hypothesized that iron-mediated intracellular hydroxyl radical formation after infection is a key event in triggering the production of interleukin-6 (IL-6) by ECs in vitro. METHODS: Cultured ECs were incubated with Fe(II) and Fe(III) or infected with Chlamydia pneumoniae or influenza A/H1N1/Taiwan/1/81 for 48 and 24 h, respectively. To determine the role of iron and reactive oxygen species, cells were coincubated with the H2O2 scavenger N-acetyl-l-cysteine, with the iron chelator deferoxamine (DFO) or with the intracellular hydroxyl radical scavenger dimethylthiourea (DMTU). After the incubation periods, supernatants were harvested for IL-6 determination. RESULTS: Incubating ECs with Fe(II) and Fe(III) resulted in increased IL-6 production. Similarly, infection with C. pneumoniae and influenza A also induced an IL-6 response. Coincubating ECs with DFO or DMTU blocked this response. Nuclear factor-kappaB activity was increased after infection and blocked by coincubation with DFO or DMTU. CONCLUSION: Cultured ECs respond to infection and iron incubation with increased production of IL-6. Iron, the generation of intracellular hydroxyl radical and NF-kappaB activity are essential in cellular activation, suggesting that reactive oxygen species generated in the Haber-Weiss reaction are essential in invoking an immunological response to infection by ECs.
PMID: 11886437 [PubMed - indexed for MEDLINE]
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time to load up on the green tea again. I have in the past taken high doses of green tea without noticing any positive or negative effect on my MS but maybe in conjunction with the ginkgo and salvia some good effects will occur.
1: J Neural Transm Suppl. 2006;(71):249-57.Links
Green tea catechins as brain-permeable, non toxic iron chelators to "iron out iron" from the brain.Mandel S, Weinreb O, Reznichenko L, Kalfon L, Amit T.
Eve Topf and US NPF Centers for Neurodegenerative Diseases and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.
mandel@tx.technion.ac.il
Evidence to link abnormal metal (iron, copper and zinc) metabolism and handling with Parkinson's and Alzheimer's diseases pathology has frequently been reported. The capacity of free iron to enhance and promote the generation of toxic reactive oxygen radicals has been discussed numerous times. Metal chelation has the potential to prevent iron-induced oxidative stress and aggregation of alpha-synuclein and beta-amyloid peptides. The efficacy of iron chelators depends on their ability to penetrate the subcellular compartments and cellular membranes where iron dependent free radicals are generated. Thus, natural, non-toxic, brain permeable neuroprotective drugs, are preferentially advocated for "ironing out iron" from those brain areas where it preferentially accumulates in neurodegenerative diseases. This review will discuss the most recent findings from in vivo and in vitro studies concerning the transitional metal (iron and copper) chelating property of green tea, and its major polyphenol, (-)-epigallocatechin-3-gallate with respect to their potential for the treatment of neurodegenerative diseases.
PMID: 17447435 [PubMed - indexed for MEDLINE
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anyone tried silicon?! I see that this can be bought at Iherb. I may purchase some.
1: Mult Scler. 2006 Oct;12(5):533-40. Links
Elevated urinary excretion of aluminium and iron in multiple sclerosis.Exley C, Mamutse G, Korchazhkina O, Pye E, Strekopytov S, Polwart A, Hawkins C.
Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK.
c.exley@chem.keele.ac.uk
Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing-remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.
PMID: 17086897 [PubMed - indexed for MEDLINE]
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milk thistle:
1: J Inorg Biochem. 2001 Jun;85(2-3):123-9. Links
Silybin, a new iron-chelating agent.Borsari M, Gabbi C, Ghelfi F, Grandi R, Saladini M, Severi S, Borella F.
Dipartimento di Chimica, Università di Modena, Via Campi 183-41100 Modena, Italy.
Silybin, a natural occurring flavolignan isolated from the fruits of Silibum marianum, has been reported to exert antioxidant and free radical scavenging abilities. It was suggested to act also as an iron chelator. The complexation and protonation equilibria of the ferric complex of this compound have been studied by potentiometric, spectrophotometric and electrochemical techniques. The formation of the complex silybin-Ga(III) in anhydrous DMSO-d6 has been studied by 1H NMR spectroscopy. Mass spectrometry and infrared spectroscopy on silybin-Fe(III) complex confirm all data obtained by 1H NMR spectroscopy. The experimental results show that silybin binds Fe(III) even at acidic pH. Different ternary complexes were observed at increasing methoxide ion concentration and their stability constants have been calculated. The results show the possible role of silybin in relation to the chelation therapy of chronic iron overload, as occurs in the treatment of Cooley's anemia.
PMID: 11410232 [PubMed - indexed for MEDLINE]
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chlorogenic acid (coffee)
1: Biosci Biotechnol Biochem. 1998 Jan;62(1):22-7. Links
Iron chelation by chlorogenic acid as a natural antioxidant.Kono Y, Kashine S, Yoneyama T, Sakamoto Y, Matsui Y, Shibata H.
Department of Life Science and Biotechnology, Faculty of Life and Environmental Science, Shimane University, Japan.
ykono@life.shimane-u.ac.jp
Chlorogenic acid, a dietary antioxidant, effectively inhibited the iron-induced lipid peroxidation of bovine liver microsomes in a concentration-dependent manner. In the Fenton-type reaction, chlorogenic acid inhibited the production of the hydroxyl radical by iron-EDTA or iron-ADP, while iron plus chlorogenic acid did not generate the hydroxyl radical. The formation of an iron complex with chlorogenic acid was demonstrated by UV/vis absorbance spectroscopic, ESR and 1H-NMR studies. The ferric complex with chlorogenic acid was in the ferric high-spin state near rhombicity, and had no radical scavenging activity. The results indicate that chlorogenic acid prevented the formation of the hydroxyl radical by forming a chelate with iron whose complex cannot catalyze the Fenton-type reaction.
PMID: 9501514 [PubMed - indexed for MEDLINE]
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Chlorogenic acid is a family of esters formed between certain trans cinnamic acids and (-)-quinic acid[1] and is a major phenolic compound in coffee, found widespread in plants, and can be isolated from the leaves and fruit.[2] This compound, long known as an antioxidant, also slows the release of glucose into the bloodstream after a meal.[3]
My bladder and bowel have improved noticeably and I can now void the bladder without manual assistance although this isn't the case every time. The bowel is much more regular. I'm sure that this is down to the salvia/ginkgo. If only I could make the reductions in spasticity I can quite often feel with the ginkgo/salvia permanent![/url][/url][/quote]