Triptolide inhibits proinflammatory factor-induced over-expression of class II MHC and B7 molecules in renal tubular epithelial cells.
AIM: To investigate the effects of triptolide on proinflammatory factor-induced over-expression of class II major histocompatibility complex (class II MHC), B7-1, B7-2, and intercellular adhesion molecule-1 (ICAM-1) in human proximal tubular epithelial (HKC) cells. METHODS: HKC cells were exposed to both interferon gamma (IFN-gamma, 200 microg/L) and tumor necrosis factor alpha (TNF-alpha, 20 microg/L) and cultured in media containing different concentrations of triptolide for 24 h. Class II MHC, B7-1, B7-2, and ICAM-1 levels in HKC cells were evaluated by flow cytometry. ICAM-1 mRNA level was measured by semi-quantitative RT-PCR method. RESULTS: HKC cells expressed quite high level of ICAM-1 and very low levels of class II MHC, B7-1, and B7-2 molecules. Class II MHC, B7-1, B7-2, and ICAM-1 levels in HKC cells were significantly increased by the costimulation of IFN-gamma and TNF-alpha. Triptolide inhibited the over-expression of class II MHC, B7-1, and B7-2 molecules in a concentration-dependent manner. The up-regulations of ICAM-1 molecules and ICAM-1 mRNA level were not altered by triptolide. CONCLUSION: Triptolide can significantly inhibit proinflammatory factors induced over-expression of class II MHC, B7-1, and B7-2 costimulatory factors in tubular epithelial cells. These results may contribute to the therapeutic effects of triptolide in some renal diseases.