EGCG改善肿瘤坏死因子-α诱导L6细胞胰岛素抵抗的实验研究  

Epigallocatechin-3-O-gaIlate inhibits tumour necrosis factor-αinduced insulin resistance in rat skeletal muscle cells

作　　者：张召锋[1] 戴小倩[1] 丁叶[1] 王军波[1] 赵明[1] 王茵[2] 李勇[1] 

机构地区：[1]北京大学公共卫生学院营养与食品卫生学系,北京100191 [2]浙江省医学科学院,杭州310013

出　　处：《中国预防医学杂志》2009年第11期973-975,共3页Chinese Preventive Medicine

基　　金：国家"十一五"科技支撑项目(2006BAD28B01)

摘　　要：目的观察表没食子儿茶素没食子酸酯(EGCG)对肿瘤坏死因子-α(TNF-α)诱导的大鼠肌细胞胰岛素抵抗的影响。方法分化好的L6肌细胞分为7组:A组(对照)、B组(100nmol/L胰岛素)、C组(10μg/LTNF-α)、D组(100nmol/L胰岛素+10μg/LTNF-α)、E组(胰岛素+TNF-α+10μmol/LEGCG)、F组(胰岛素+TNF-α+20μmol/LEGCG)、G组(胰岛素+TNF-α+40μmol/LEGCG),继续培养24 h。实验结束后采用葡萄糖转运实验检测胰岛素刺激下L6细胞对葡萄糖的利用情况,Western blot检测细胞胰岛素受体底物-1(IRS-1)和AMP激活的蛋白激酶(AMPK)的蛋白表达水平。结果与100 nmol/L胰岛素组比较,10μg/L TNF-α作用24h后胰岛素刺激下细胞内葡萄糖转运量明显减少(P<0.05),而EGCG作用后明显改善TNF-α的抑制作用(P<0.05),并呈剂量反应关系。Western blot结果显示,与胰岛素组相比,TNF-α增高IRS-1的Ser307磷酸化表并降低AMPK的磷酸化水平,而EGCG作用后减少IRS-1的Ser307磷酸化表达同时升高AMPK的磷酸化水平。结论10μg/L TNF-α作用24 h能诱导L6肌细胞的胰岛素抵抗,而EGCG能改善这种胰岛素抵抗,可能是通过减少IRS-1的Ser307磷酸化进而增加AMPK的磷酸化表达来实现的。Objective To investigate the effects of epigallocatechin-3-O-gallate （EGCG） on insulin resistance in rat L6 cells treated with tumor necrosis factor α （TNF-α）. Methods EGCG was coincubated with TNF-α-treated rat L6 cells for 24 h. The glucose uptake of 1.6 cells was studied by [^3H]-2-deoxyglucose uptake assay. Insulin receptor substrate-1 （IRS-1） and AMP-activated protein kinase （AMPK） levels were examined by western blotting. Results TNF-α increased Ser307 phosphorylation of insulin receptor substrate-1 （ IRS-1 ） and reduced phosphorylation of AMPK. Furthermore, glucose uptake was inhibited by TNF-α, while EGCG treatment improved insulin-stimulated glucose uptake. It was demonstrated that these effects of EGCG were essentially depended on the AMPK activation. Conclusion These results suggest that EGCG inhibits TNF-α-induced insulin resistance through AMPK pathway.

关 键 词：EGCG 肿瘤坏死因子-Α 胰岛素抵抗 

分 类 号：R587[医药卫生—内分泌]