Immunosuppressive effect of triptolide in vitro

Lü, Hua; Hachida, M; Enosawa, Shin; Li, X.-K; Suzuki, Seiichi; Koyanagi, Hitoshi

doi:10.1016/s0041-1345(99)00262-6

Cited by 38 publications

(23 citation statements)

References 2 publications

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“…The immunosuppressive effects of TRI can be partially attributed to its potent inhibition of T cell activation and interleukin-2 production [21] . Remarkably, the inhibitory effect of TRI on T cell activation has been shown to be more potent than that exhibited by cyclosporine [22] and Tacrolimus (FK-506) [23] . MPO is a specific enzyme in the cytoplasm of neutrophils, which induces the activation and aggregation of neutrophils.…”

Section: Discussionmentioning

confidence: 99%

Triptolide inhibits NF-κB activation and reduces injury of donor lung induced by ischemia/reperfusion

Zhu

et al. 2007

Acta Pharmacologica Sinica

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Aim: To investigate the protective effect of triptolide (TRI) on ischemia/reperfusioninduced injury of transplanted rabbit lungs and to investigate the mechanisms underlying the actions of TRI. Methods: We established the rabbit lung transplantation model and studied lung injury induced by ischemia/reperfusion and the inhibitory effect of TRI on NF-κB. The severity of lung injury was determined by a gradual decline in PvO 2 , the degree of lung edema, the increase in the myeloperoxidase (MPO) activity, and the ultrastructural changes of transplanted lungs. The activation of NF-κB was measured by immunohistochemistry. The increase in intercellular adhesion molecule-1 (ICAM-1), which is the target gene of NF-κB, was evaluated by ELISA. Results: After reperfusion, there was a gradual decline in the PvO 2 level in the control group (group I). The level of PvO 2 in the group treated with lipopolysaccharide (group II) was significantly decreased, whereas that of the group treated with TRI (group III) was markedly improved (P<0.01). In group III, the activity of MPO was downregulated, and the pulmonary edema did not become severe and the ultrastructure of the donor lung remained normal. The activity of NF-κB and the expression of ICAM-1 was significantly increased in the donor lungs. TRI blocked NF-κB activation and ICAM-1 expression. Conclusion: The effects of TRI on reducing injury to donor lungs induced by ischemia/reperfusion may possibly be mediated by inhibiting the activity of NF-κB and the expression of the NF-κB target gene ICAM-1. Thus, TRI could be used in lung transplantations for improving the function of donor lungs.

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Section: Discussionmentioning

confidence: 99%

Triptolide inhibits NF-κB activation and reduces injury of donor lung induced by ischemia/reperfusion

Zhu

et al. 2007

Acta Pharmacologica Sinica

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“…1A) (16). This natural product, isolated from the medicinal vine Tripterygium wilfordii Hook F (''Thunder God Vine'') and used in traditional Chinese medicine for centuries, has a myriad of therapeutic uses against cancer, inflammation, and autoimmune diseases (17)(18)(19). Triptolide has been shown to induce apoptosis or cell growth arrest depending on its concentration and the cell type treated (16,(20)(21)(22).…”

mentioning

confidence: 99%

Triptolide is a traditional Chinese medicine-derived inhibitor of polycystic kidney disease

Leuenroth

Okuhara²,

Shotwell

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

213

156

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During kidney organogenesis, tubular epithelial cells proliferate until a functional tubule is formed as sensed by cilia bending in response to fluid flow. This flow-induced ciliary mechanosensation opens the calcium (Ca 2؉ ) channel polycystin-2 (PC2), resulting in a calcium flux-mediated cell cycle arrest. Loss or mutation of either PC2 or its regulatory protein polycystin-1 (PC1) results in autosomal dominant polycystic kidney disease (ADPKD), characterized by cyst formation and growth and often leading to renal failure and death. Here we show that triptolide, the active diterpene in the traditional Chinese medicine Lei Gong Teng, induces Ca 2؉ release by a PC2-dependent mechanism. Furthermore, in a murine model of ADPKD, triptolide arrests cellular proliferation and attenuates overall cyst formation by restoring Ca 2؉ signaling in these cells. We anticipate that small molecule induction of PC2-dependent calcium release is likely to be a valid therapeutic strategy for ADPKD.ADPKD ͉ calcium ͉ natural product ͉ polycystin ͉ renal cyst

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“…[2][3][4] The ethanol extract, ethyl acetate extract, and other extracts of TWHf containing triptolide have been used for the treatment of rheumatoid arthritis and autoimmune diseases clinically and triptolide was deemed to account for the immunosuppressive activity of the extracts. [5][6][7] However, triptolide has severe toxicities on digestive, urogenital, and blood circulatory systems, 8,9) which have largely limited its clinical application.…”

mentioning

confidence: 99%

Involvement of Mitochondrial Pathway in Triptolide-Induced Cytotoxicity in Human Normal Liver L-02 Cells

Yao

Jiang

Duan³

et al. 2008

Biological & Pharmaceutical Bulletin

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Immunosuppressive effect of triptolide in vitro

Cited by 38 publications

References 2 publications

Triptolide inhibits NF-κB activation and reduces injury of donor lung induced by ischemia/reperfusion

Triptolide inhibits NF-κB activation and reduces injury of donor lung induced by ischemia/reperfusion

Triptolide is a traditional Chinese medicine-derived inhibitor of polycystic kidney disease

Involvement of Mitochondrial Pathway in Triptolide-Induced Cytotoxicity in Human Normal Liver L-02 Cells

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