| Aims: It is obvious that the activation and proliferation of hepatic stellate cells(HSC) is a key event in hepatic fibrogenesis. For its anti-fibrogenic activity, interneukin-10(IL-10) is proposed as one of therapeutics for liver fibrosis. HSC actived by culture in vitro and advancedly actived by platelet-derived growth factor(PDGF) were treated with IL-10 in the present study. Proliferation, apoptosis, contraction of HSC and expression of fibrogenic cytokines in HSC was observed to investigate the anti-fibrotic mechanisms of IL-10.Methods: A rat HSC cell line cultured in vitro was exposed in IL-10 and/or PDGF. The contraction of HSC was observed with micscope, the proliferation was measured by MTT, and the expression of collagen type I and type III, transforming growth factor-β1(TGF-β1), epidermal growth factor(EGF), fibroblast growth factor(FGF) and Fas/FasL was respectively measured by semiquantitative reverse-transcription polymerase chain reaction(RT-PCR) and immunocytochemistry on each group.Results: IL-10 remarkably increased the expression of FasL but not Fas in HSC, and significantly but slightly inhibited the proliferation of HSC and the expression of TGF-β1 and FGF in HSC. PDGF markedly promoted the contraction and proliferation of HSC as well as the expression of collagen type I and type III, TGF-β1 and FGF in HSC. This promotion was significantly inhibited by IL-10.Conclusions: The anti-fibrotic mechanisms of IL-10 partly due to its upregulation on FasL expression which leads to apoptosis of HSC and its inhibition on the promotion of PDGF on proliferation, contraction of HSC,and the expression ofcollagen type I and type III, TGF-β1 and FGF in HSC.
|
PDF Full Text Request