非酒精性脂肪性肝炎发病机制的实验研究

Experimental study on the pathogenesis of nonalcoholic steatohepatitis

建立大鼠非酒精性脂肪性肝炎 (NASH)动物模型 ,探讨NASH发病机制。雄性SD大鼠随机分为对照组及模型组 ,检测血清转氨酶、空腹血糖 (FBG)、胰岛素 (FBI)及肿瘤坏死因子α(TNFα)水平 ,肝组织匀浆MDA、SOD水平 ,肝组织学改变。于 9周末模型组大鼠已产生胰岛素抵抗 ,血清TNFα水平明显升高 ,肝细胞出现脂肪变及气球样变 ;14周末血清转氨酶水平及肝组织匀浆MDA水平明显升高 ,SOD水平明显下降 ,肝组织出现炎细胞浸润。胰岛素抵抗与TNFα在肝脏脂肪变的发生中起到重要作用 。

To explore the pathogenesis of nonalcoholic steatohepatitis in model rats. 40 male SD rats were randomly allocated into 4 groups. Normal rats were red with general diet. Model rats were fed with high fat diet. After fed 9 and 14 weeks, the rats were put to death. Blood serum transaminase, glucose, insulin, TNF-α level and liver constitution homogenate MDA, SOD level and liver histology were detected. After 9 weeks, model rats developed insulin resistance, blood serum TNFα level were markedly increased and the livers presented the pathology of hepatocyte steatosis. After 14 weeks, transaminase level, and liver constitution homogenate MDA were increased, SOD level was markedly decreased and livers presented the pathology of inflammation cell infiltration. Insulin resistance and TNFα play a key role in occurrence of hepatocyte steatosis; Lipid peroxidation has intimate relation with inflammation.