白藜芦醇对大鼠非酒精性脂肪肝的作用及机制研究

被引:19
作者
王晓珂 [1 ]
赵健亚 [2 ]
刘天娥 [1 ]
蒋建中 [1 ]
张璇 [1 ]
王春 [1 ]
陈刚 [1 ]
机构
[1] 南通大学公共卫生学院环境卫生学教研室
[2] 南通大学公共卫生学院营养与食品卫生学教研室
关键词
白藜芦醇; 非酒精性脂肪肝; 腺苷酸激活蛋白激酶; 葡萄糖转运蛋白4; 固醇调节元件结合蛋白-1c;
D O I
10.16421/j.cnki.1002-3127.2013.06.021
中图分类号
R285.5 [中药实验药理];
学科分类号
100806 [中药药理学];
摘要
目的观察白藜芦醇对高脂膳食诱导的大鼠非酒精性脂肪肝的作用并探讨相关的分子机制。方法 63只6周龄雄性SD大鼠随机分为高脂组和普通饲料组,8周后通过体重和肝脏病理切片建立非酒精性脂肪肝(NAFLD)模型。再将NAFLD组大鼠随机分为模型组和白藜芦醇干预组(250 mg/kg·bw)。干预结束后,称取大鼠体重、体脂和肝脏重量,分离血清测定相关指标,病理切片观察肝脏的脂肪蓄积,实时定量PCR检测肝脏腺苷酸激活蛋白激酶(AMPK)/沉默静息因子(Sirt1)通路基因的表达。结果白藜芦醇干预结束后,干预组大鼠的体重、体脂比、肝重、肝脏系数和肝脏脂肪蓄积量与模型组相比显著降低(P<0.05);天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)的含量和胰岛素抵抗指数(HOMA-IR)与模型组相比也显著降低,高密度脂蛋白胆固醇(HDL-C)的含量显著增加(P<0.05);与模型组相比,干预组AMPKα1、AMPKα2、Sirt1和葡萄糖转运蛋白4(GLUT4)的mRNA表达显著增加,固醇调节元件结合蛋白-1c(SREBP-1c)mRNA表达显著降低。结论白藜芦醇可能通过促进AMPKα、Sirt1和GLUT4的表达改善胰岛素敏感性,抑制SREBP-1c的表达降低脂质沉积改善高脂膳食诱导的非酒精性脂肪肝。
引用
收藏
页码:450 / 453
页数:4
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