应用高脂饮食饲养Wistar大鼠建立非酒精性脂肪肝病（non-alcoholic fatty liver disease，NAFLD）肝纤维化体内模型, 选用重组抵抗素作用于肝星状细胞(hepatic stellate cell-t6, HSC-T6)建立体外模型。观察肝组织纤维化的情况；检测体内体外Ⅲ型前胶原(PCⅢ)、透明质酸(HA)、Ⅳ型胶原(CIV)、层黏蛋白(LN)水平；检测肝组织抵抗素mRNA和蛋白的表达水平；检测HSC-T6中转化生长因子β-1(TGF-β1) mRNA及肿瘤坏死因子α(TNF-α) mRNA表达水平。结果显示, 随着高脂喂养时间的延长, 大鼠肝组织抵抗表达逐渐增加且纤维化程度逐渐加重; 随着抵抗素浓度的增加, HSC-T6上清中纤维化指标升高, 细胞中TGF-β1 mRNA及TNF-α mRNA表达增加。与对照组比较, 各指标差异均有显著性(P<0.05或0.01)。上述结果显示抵抗素通过TNF-α、TGF-β1诱导NAFLD肝纤维的发生和发展
To investigate the effects and possible mechanisms of resistin on hepatic fibrosis in non-alcoholic fatty liver disease, this review used an in vivo model utilizing Wistar rats with a high fat diet. Recombinant resistin was selected to play role in hepatic stellate cells in the HSC-T6 cell line. We observed the degrees of hepatic ?brosis, measured the levels of Liver fibrosis spectrum and detected expression levels of resistin mRNA and protein in liver tissue as well as the expression levels of TGFβ-1 and TNF-α mRNA in HSC-T6. The results showed that expression of resistin in rat liver tissue and the degree of hepatic fibrosis increased over time with a high fat diet. Along with the increased concentration of resistin and levels of fibrosis index, TGFβ-1and TNF-α also increased in HSC-T6 cells. Compared with the control group, significant differences were found between each group, suggesting resistin by proinflammatory cytokine TNF-α and TGF-β1 induced the occurrence and development of NAFLD in hepatic fibrosis.