Abstract: ［Abstract］ Objective〖HTSS〗〓To explore whether Krüppellike factor 5（KLF5） was involved and the mechanism in high glucoseinduced inflammation in vascular smooth muscle cells(VSMCs).
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓VSMCs were cultured with different concentrations of glucose or treated with high glucose for various times, quantitative realtime polymerase chain reaction(qRTPCR) and Western blot were performed to examine the expression of tumor necrosis factorα(TNFα), KLF5 and NFκB p50. Endogenous KLF5 was knocked down by transfecting VSMCs with KLF5specific siRNA or nonspecific siRNA, and then treated the cells with or without high glucose, Western blot was performed to examine the expression of TNFα. VSMCs were cultured in medium containing 5.5 mmol/L or 25 mmol/L glucose. The cell lysates were immunoprecipitated With antiKLF5 or antiNFκB p50 antibody, and the resulting precipitates were analyzed by Western blot using antiNFκB p50 or antiKLF5 antibody.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓In mRNA and protein levels, high glucose increased the level of TNFα, KLF5 and NFκB p50 in a dose and timedependent manner in VSMCs（P＜005）. When knocked down endogenous KLF5, the results of Western blot suggested that high glucoseinduced TNFα expression was mediated by KLF5. The results of coimmunoprecipitation experiments showed that exposure of high glucose increased the interactions of KLF5 and NFκB p50.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓KLF5 and NFκB p50 interactions induced by high glucose cooperatively induce proinflammatory gene expression.

Key words: vascular smooth muscle cells, Krüppellike factor 5, nuclear factor κB p50