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.
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.
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. firstname.lastname@example.org
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.
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.
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. email@example.com
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.
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. firstname.lastname@example.org
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.
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. email@example.com
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
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.
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.
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.
What is that then?
Titre du document / Document titlehttp://cat.inist.fr/?aModele=afficheN&cpsidt=17569319
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
What is ren shen yang rong tang?
ren shen yang rong tang 人 參 養 榮 湯http://alternativehealing.org/ren_shen_yang_rong_tang.htm
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
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
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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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.