【Abstract】 Objective To study the role of antiinflammatory of HSF2 through overexpressed and knockeddown on inflammatory reaction and its mechanism of human colonic epithelial cell.Methods Caco2 cells were transfected with HSF2 siRNA and recombinant plasmid (pCMVHSF2FLAG) using Lipofectamine. Cytotoxicity was estimated by the MTT (3［4,5dimethyl2thiazol2yl］2,5diphenyltetrazolium bromide) assay. After LPS stimulated the different treatment cells, Nitric oxide (NO) were measured by Griess reagent. The protein and mRNA expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase2 (COX2), tumor necrosis factora (TNFa) and interleukin8 (IL8) were analysed by Western Blot, ELISA and RTPCR, respectively. Phosphorylation levels ofextracellular signalregulated kinase 1/2 (ERK1/2), cJun Nterminal protein kinase (JNK) and p38 mitogenactivated protein kinase (p38 MAPK) , inhibitor κBa (IκBa) and nuclear factorκB p65 (NFκBp65) were measured by Western Blot. Results The cell by treated by Lipofectamine means did not decrease the viability of Caco2 cells. Silenced HSF2 significantly attenuated the LPSinduced expression of NO, iNOS, COX2, TNFa, IL8 in Caco2 cells(P＜005). In addition, It increased phosphorylation of IκBa, NFκB, JNKand p38,but decreased ERK1/2. The effect of overexpressed HSF2 on the above index4s was contrary.Conclusion This study indicates that HSF2 inhibited LPSinduced proinflammatory enzymes and proinflammatory cytokines via upregulation ERK1/2, but, downregulation phosphorylation of JNK, p38 MAPK and NFκB pathways. HSF2 has a potential antiinflammatory properties , might be a new clue to reveal the pathogenesis of UC and a new target for intervention in the inflammatory response .