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Triptolide is the major bioactive constituent extracted from the Chinese herb Tripterygium wilfordii.

Triptolide inhibit the expression of IL-2 in activated T cells and NF-κB mediated transcription activation [1]. Triptolide also can inhibit colony formation and the proliferation of tumor cells at extremely low concentrations.

Triptolide treatment at the concentration of 15 nM inhibited the invasion and migration of ovarian cancer cells SKOV3 and A2780. Triptolide inhibited MMP7 and MMP19 expression with a dose-dependent manner from 0 to 15 nM in ovarian cancer cells. Triptolide also enhanced expression of the E-cadherin in ovarian cancer cell, then, affected the migration and cell invation.[2] Triptolide triggered a CDK7-mediated degradation of RNAPII, including its robust anticancer properties. Triptolide induced Rpb1 decrease with a dose-dependent manner at lowest 100 nM, resulting to a significant RNAPII reduction in SKOV3 cells.[3] Triptolide caused significant decrease of cell viability in a dose-dependent manner with IC50 value of 74.3 nM in RSF (rheumatoid synovial fibroblasts). Triptolide also has inhibition effect on cell proliferation in RSF with IC50= 20.4 nM. Treatment with triptolide (100 nM) for 24 h caused distinctive morphological changes in synovial cells.[4] Triptolide induces apoptotic death of peripheral T cells and T cell hybridomas by increase of DEVD-cleavable caspases activity at 10-100 ng/ml.[5]

Triptolide also inhibited cytokine-induced MMP-3 expression at 125-150nM in primary human synovial fibroblasts, SW1353 cells, and human OA chondro-cytes protecting artilage from aggrecanase- and MMP -driven breakdown.[6]

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