【摘要】 [目的]观察小檗碱对游离脂肪酸诱导的HepG2细胞胰岛素抵抗模型AMPK信号通路蛋白及其下游糖脂代谢关键蛋白表达的影响,探讨小檗碱改善胰岛素抵抗的分子机制。[方法]软脂酸诱导HepG2细胞建立胰岛素抵抗模型,予以不同浓度的小檗碱进行干预,同时以AICAR作为阳性对照,Compound C作为阴性对照,用葡萄糖氧化酶法检测葡萄糖消耗量,甘油三酯试剂盒检测细胞内的甘油三酯含量,Western blot检测LKB1、AMPK、TORC2、PEPCK、G-6-P、P-ACC、ACC、FAS蛋白表达。[结果]软脂酸作用24h使HepG2细胞葡萄糖消耗量显著下降,TG含量显著增加,LKB1、AMPK及P-ACC蛋白表达明显减少,TORC2、PEPCK、G-6-P、ACC、FAS蛋白表达明显增加;而小檗碱或AICAR则可逆转上述效应。[结论]小檗碱可以有效改善软脂酸诱导的胰岛素抵抗,其分子机制可能与小檗碱调控AMPK信号通路相关蛋白的表达有关。更多还原

【Abstract】 [Objective]To reveal the molecular mechanism of berberine on improving insulin resistance by observing the effects of berberine on the expression of AMPK signaling pathway and downstream glucolipid metabolism related key proteins in insulin-resistant HepG2 cells induced by free fatty acid.[Methods]HepG2cells were treated with palmitic acid to induce insulin resistance and intervened with different concentrations of berberine,meanwhile,AICAR was used for positive control as well as Compound C used for negative control.Glucose consumption was assayed through glucose oxidase method and the amount of triglycerides was measured by Triglyceride Assay kit.The expression of LKB1,AMPK,TORC2,PEPCK,G-6-P,P-ACC,ACC,FAS protein was detected by Western blot.[Results]Treatment with palmitic acid for 24 hours made glucose consumption of HepG2 cells substantially reduced and triglyceride content markedly increased.Besides,the expression of LKB1,AMPK and their primary downstream targeting enzyme P-ACC reduced obviously,while the expression of TORC2,ACC,FAS and gluconeogenic limiting enzymes PEPCK and G-6-P increased apparently.However,the aforementioned indices were reversed bytreatment with berberine or AICAR.[Conclusion]Berberine can effectively improve the insulin resistance induced by palmitic acid in HepG2 cells.Its molecular mechanism may be associated with regulating AMPK related signal pathway proteins expression.更多还原