姜黄素干预非酒精性脂肪肝的差异蛋白质组学研究

目的:基于差异蛋白质组学研究姜黄素对高脂肪饮食诱导的非酒精性脂肪肝模型大鼠的作用机制。方法:雄性Wistar大鼠30只,随机分为正常组、模型组和姜黄素组;模型组和姜黄素组以高脂饮食12周诱导大鼠脂肪肝,同时姜黄素组予姜黄素灌胃,模型组予等体积助溶剂灌胃。至12周处死大鼠,收集血清及肝组织样本。分别检测血清丙氨酸氨基转氨酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆固醇(TC)水平,肝组织γ-谷氨酰转移酶(γ-GT)和三酰甘油(TG)含量。采用双向凝胶电泳技术分离肝组织总蛋白,运用串联飞行时间质谱鉴定差异蛋白质。结果:与正常组比较,模型组大鼠血清ALT、AST、TC水平和肝组织TG、γ-GT含量均明显升高,姜黄素干预后能明显降低各指标水平。双向凝胶电泳后各组蛋白质组图谱经PDQuest软件分析鉴定得到差异蛋白点30个,经串联飞行时间质谱鉴定共获得有意义蛋白质20个,主要是线粒体功能相关酶类蛋白和细胞骨架蛋白。结论:姜黄素能显著降低高脂饮食诱导的非酒精性脂肪肝血清学指标,其机制与调节线粒体功能和维持肝细胞正常结构有关。

Differential Proteomics Analysis of Curcumin for Non-alcoholic Fatty Liver Disease in Rats

Objective: On the basis of proteomics,this paper researches the mechanism of curcumin in rats with non-alcoholic fatty liver disease(NAFLD) induced by high fat diet.Methods: Thirty male Wistar rats were randomly divided to three groups: normal group,model group and curcumin group.Rats in the model group and curcumin group were fed with high fat diet for 12 weeks to induce NAFLD,and simultaneously administered with curcumin in curcumin group,and with equal amount of cosolvent in model group.At the end of 12 weeks,all rats were sacrificed and their blood and liver tissue samples were collected.The levels of serum alkaline aminotransferase(ALT),aspartate aminotransferase(AST) and total cholesterol(TC) in serum and contents of triglyceride(TG) and gamma glutamyltransferase(γ-GT) in liver tissues were detected.Total protein in liver tissues was isolated by two-dimensional gel electrophoresis(2-DE),and some differentially expressed protein spots were analyzed and identified by flight mass spectrometry.Results: Compared with the normal group,the levels of ALT,AST,TC,TG and-GT in model group were significantly increased,and were significantly decreased after intervention of curcumin.The results of PD Quest software showed that there were 30 protein spots by 2-DE,and 20 significant proteins were detected by flight mass spectrometry,including mitochondrial function relevant enzymes protein and cytoskeleton protein.Conclusion: Curcumin can reduce serum indexes in NAFLD induced by high fat diet by regulating mitochondrial function and maintaining the structure of liver cells.