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目的：研究PPAR-γ在非酒精性脂肪性肝病（NAFLD）大鼠肝脏组织中的表达,探讨非酒精脂肪性肝病可能的发病机制。方法：雄性SD 大鼠30 只，随机分为A（正常组）15 只普通饮食，B（高脂组）15 只高脂饮食。8 周后，自两组各随机抽取2 只大鼠处死，光镜观察证实脂肪肝造模成功，继续喂养4 周后处死所有大鼠，取血清做免疫生化检查，取肝组织标本，分别以光镜观察做出 NAS 评分，免疫组化和PCR 法检测肝组织PPAR-γ蛋白的表达。结果：1.高脂饮食可以成功的复制NAFLD 的大鼠模型；2.血清 GLU、TC、TG、HDL-C、LDL-C 在高脂组表达量较正常组明显升高，差异具有统计学意义（P＜0.05）；3. 免疫组化显示：高脂组 PPAR-γ表达量较正常组升高；结论：1.高脂饮食可成功复制NAFLD 模型；2.PPAR-γ 在NAFLD 大鼠肝脏成脂性改变中具有重要作用。

英文摘要:

Objective: To investigate the expression of PPAR-gamma in nonalcoholic fatty liver disease (NAFLD) rats induced by high-fat feeding, and to investigate the possible mechanism of NAFLD. Methods: Thirty male SD rats were divided into two groups: Group A (normal group), fifteen rats were fed with normal diet; Group B (fatty group), fifteen rats were fed with high fat diet; 8 weeks later, two rats randomly selected from each group were sacrificed. Histological pathology showed that the NAFLD was established. All rats were sacrificed four weeks later. Serum was preserved for biochemical assay. Liver tissue were detected under light microscopy after HE staining. Expression of PPAR-γ protein and mRNA in hepatic cell were detected by immunohistochemistry. Results: 1. NAFLD model can be successfully replicated by high-fat diet 2.Compared with that in the control group, serum level of HDL-C, LDL-C, TC, TG, Glu of model group increased significantly（P < 0.05）;3. The expression of PPAR-γ in the fatty group was higher than that in the normal group. Conclusions: 1. NAFLD model can be replicated successfully by high-fat diet 2. PPAR-gamma play the aliphaticcompound effect in the NAFLD rats.

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