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目的探讨解耦联蛋白2(UCP2)在肝纤维化形成过程中的作用及其发生机制。方法体内实验采用四氯化碳(CCl4)诱导肝纤维化模型,取肝脏观察病理变化,用Western blotting、免疫组织化学和Real-time PCR等方法检测UCP2和p38丝裂素活化蛋白激酶(p38MAPK)的表达水平;体外实验采用UCP2特异性抑制剂京尼平和CCl4刺激星形细胞,检测UCP2和p38MAPK相关蛋白的表达情况。结果与正常组相比,模型组大鼠肝脏α-平滑肌肌动蛋白(α-SMA)和UCP2表达增高(P<0.05,n=10);加入CCl4刺激细胞后,星形细胞α-SMA表达增加,p38MAPK及其磷酸化水平增高(P<0.05,n=6);而在加入京尼平后,α-SMA表达增加,p38 MAPK及其磷酸化水平明显降低(P<0.05,n=6)。结论 UCP2参与了肝纤维化的发生,可能促进了星形细胞的活化及增殖过程。
Objective To investigate the role of uncoupling protein 2 (UCP2) in the pathogenesis of hepatic fibrosis and its mechanism. Methods Liver fibrosis was induced by carbon tetrachloride (CCl4) in vivo. Pathological changes of the liver were observed. Western blotting, immunohistochemistry and Real-time PCR were used to detect the expression of p38MAPK, . In vitro, UCP2-specific inhibitor genipin and CCl4 were used to stimulate astrocytes to detect the expression of UCP2 and p38MAPK related proteins. Results Compared with the normal group, the expression of α-smooth muscle actin (α-SMA) and UCP2 increased (P <0.05, n = 10) in the model group; α-SMA expression of astrocytes (P <0.05, n = 6). However, after the addition of genipin, the expression of α-SMA increased and the phosphorylation of p38 MAPK and p38 MAPK decreased significantly (P <0.05, n = 6 ). Conclusion UCP2 is involved in the pathogenesis of hepatic fibrosis and may promote the activation and proliferation of astrocytes.