| Objective: It is obvious that hepatic stellate cells (HSC) are the major source of extracellular matrix production and deposition,and the activating of HSC plays a central role in liver fibrosis . Many studies indicate that IL-10 has a close relation with the pathogenesis of chronic liver injury, also it has antifibrogenic action. A rat rHSC- 99 cell line cultured in vitro was exposed in IL-10 and/or TGFβ1 in present study. The expression of type I procollagen ,TIMP-1 and MMP-2 in HSC was observed to investigate the antifibrogenic mechanisms of IL-10.Methods: A rat rHSC-99 cell line cultured in vitro was exposed in IL-10 and/or TGFβ1.The synthesis of type I procollagen was measured by enzyme-linked immunoadsordent assay (ELISA). The expression of TIMP-1 and MMP-2 was respectively measured by semiquantitative reverse-transcription polymerase chain reaction (RT-PCR). Results: TGFβ1 remarkably increased the expression of type I procollagen ,TIMP-1 and MMP-2 in HSC.The expression of type I procollagen ,TIMP-1 and MMP-2 has no remarkable change when HSC was only exposed in IL-10. But IL-10 significantly inhibited the expression of type I procollagen and TIMP-1 mediated by TGFβ1 .Conclusions: TGFβ1 remarkably increased the expression of type I procollagen ,TIMP-1 and MMP-2 in HSC. The antifibrogenic action of IL-10 is partly due to its inhibition on the promotion of the expression of of type I procollagen and TIMP-1 mediated by TGFβ1 . |