To inv estigate the effects of triptolide in in hibiting the MCP-1 production in human p roximal tubular cells. METHO DOLOGY A human proximal tubu lar cell line was selected.A combination of IFN-γ(200 μg/L)and TNFα(20 μg/L)was used to stimulate the production of MCP- 1 in tubular cells.Intracellular MCP-1 w as detected by flowcytometry and MCP-1 i n the supernatant was measured by “sandw ich” ELISA method.MCP-1 mRNA expression was detected by semi-quantitative polyme rase chain reaction. RESULTS In unstimulated tubular cel ls,a mild of MCP-1 was detected in cells and in culture supernatants.In the supe rnatants of tubular cells costimulated with IFN-γ(200 μg/L)and TNFα(20 μg/L)for 24 hours,MCP-1 production was significa ntly increased (1120.9±71.9 vs 141.9±1 7.3 ng/L·μg protein -1,P<0.01),a simi lar increase of intrac ellular MCP-1 protein was observed with FA CS analysis.MCP-1 mRNA expression was in creased nearly two folds of that in uns tim ulated cells.Triptolide could dose-depen dently inhibit MCP-1 protein production( 713.1±28.4 vs 1120.9±71.9 ng/L·μg prot ein -1,P<0.01)and mRNA expression sti mulated by inflammatory factors. CONCLUSION Triptolide can inhibit M CP-1 overproduction in human tubular cel ls induced by IFN-γ(200 μg/L)and TNFα(20 μg/L)costimulation.This may be one of t he mechanisms by which triptolide excert s in treatment of renal diseases.