高血糖对肝纤维化大鼠肝组织α—SMA和CTGF表达的影响

目的探讨高血糖对肝纤维化大鼠肝组织α－平滑肌肌动蛋白（α－SMA反映肝星状细胞HSC活化）和结缔组织生长因子（CTGF）表达的影响。方法将52只SD雄性大鼠随机分为糖尿病肝纤维化组、正常血糖肝纤维化组与正常对照组。通过链脲佐菌素（streptozocin，STZ）诱导糖尿病，后用四氯化碳诱导肝纤维化。肝组织HE染色检测病理改变。免疫组化法检测肝组织α－SMA、CTGT蛋白表达。结果高血糖肝纤维化组α—SMA（灰度值142．5±3．67）和CTGF（灰度值144．2±5．01）表达水平较正常血糖肝纤维化组（α—SMA灰度值158．9±2．18，CTGF灰度值157．7±6．80）显著升高（P〈0．05）。结论高血糖可通过诱导肝脏α—SMA、CTGF表达，加重大鼠肝纤维化的程度，促进肝纤维化的形成。其机制与促进肝星状细胞的增殖活化及细胞外基质的合成分泌等有关。

Effect of hyperglycemia on the expression of α-SMA and CTGF in rats with hepatic fibrosis

Objective To study the effects of hyperglycemia on the expression of α-SMA （indication of activation with hepatic stellate cell）and CTGF in rats with hepatic fibrosis. Methods 52 male SD rats were randomly divided into 3 groups： diabetic hepatic fibrosis group, hepatic fibrosis group of normal blood glucose and normal group. Diabetic group was induced by STZ （60 mg/kg）. Hepatic fibrosis were induced by CC14 （40%,2 ml/kg,twice in a week） after hyperglycemia. The liver tissue pathology change was detected with HE staining. The protein expression of CTGF andα-SMA in rats＇ liver tissue were detected with immunohistochemistry. Results Compared with hepatic fibrosis group of normal blood glucose group,the expression levels of α-SMA and CTGF increased obviously in diabetic group（P〈0.05）. Conclusion Hyperglycemia may aggravate progression of hepatic fibrosis by inducing expression of α-SMA and CTGF.The mechanism may be related with promoting activation of hepat- ic stellate cell and extra cellular matrix （ECM） synthesis and secretion.