复方贞术调脂方对游离脂肪酸诱导的胰岛素抵抗HepG2细胞的作用  

Effect of FTZ on insulin-resistant HepG2 cells induced by FFA

作　　者：韩宗余[1] 贝伟剑[1] 黎明[1] 胡旭光[1] 

机构地区：[1]广东药学院国家中医药管理局高脂血症"调肝降脂"重点研究室/国家中医药管理局"脂代谢"三级实验室/广东省代谢性疾病中医药防治重点实验室,广东广州510006

出　　处：《广东药学院学报》2015年第3期349-353,共5页Academic Journal of Guangdong College of Pharmacy

基　　金：国家自然科学基金(81173626);广东省自然科学基金团队项目(10351022401000000);广东省教育部产学研结合项目(2011B090400379)

摘　　要：目的探讨复方贞术调脂方(FTZ)对游离脂肪酸(FFA)诱导的胰岛素抵抗Hep G2细胞NF-κBIRS1-GLUT4通路的影响,阐明FTZ缓解胰岛素抵抗的作用机制。方法采用FFA诱导Hep G2细胞使其产生胰岛素抵抗,3个剂量的FTZ干预后,葡萄糖氧化酶法检测Hep G2细胞培养液上清液中葡萄糖的含量,酶联免疫法检测Hep G2细胞培养液上清液中TNF-α、IL-6的含量,Western blot检测Hep G2细胞中NF-κB、IRS1、GLUT4蛋白表达,采用PDTC阻断NF-κB蛋白,测定其下游靶点IRS1的蛋白表达。结果FTZ可降低细胞上清液中葡萄糖、TNF-α、IL-6的含量,下调NF-κB的蛋白表达,上调IRS1和GLUT4的蛋白表达。阻断NF-κB之后,再加入FTZ,IRS1的蛋白表达量较未阻断时显著降低。结论 FTZ可改善FFA诱导的胰岛素抵抗,其作用机制可能是通过抑制NF-κB介导的IRS1-GLUT4通路来改善胰岛素抵抗。NF-κB是FTZ作用的关键靶点。Objective To study the effect of Fufang Zhenzhu Tiaozhi formula（ FTZ） on insulin-resistant Hep G2 cells induced by free fatty acid（ FFA） via NF-κB-IRS1-GLUT4 pathway. Methods Insulin-resistant Hep G2 cells were induced by FFA and treated with FTZ at three different dosages. The levels of glucose,TNF-α and IL-6 in culture supernatant were measured. The expressions of NF-κB,IRS1 and GLUT4 were determined by western blotting. NF-κB activity was blocked by PDTC and IRS1 expression was identified. Results FTZ treatment reduced the levels of glucose,TNF-α and IL-6 and enhanced the expression of IRS1 and GLUT4. FTZ reduced NF-κB expression in insulin-resistant Hep G2 cells. After blocked NF-κB,the expression of IRS1 protein had no obvious change when treated with FTZ. Conclusion Regulation of IRS1-GLUT4 pathway via NF-κB may be the underlying mechanism of FTZ on insulin resistance. Therefore,NF-κB is a key target of FTZ for relieving insulin resistance.

关 键 词：复方贞术调脂方 胰岛素抵抗 游离脂肪酸 核因子-ΚB 

分 类 号：R285[医药卫生—中药学]