吡格列酮对L6肌细胞脂联素和葡萄糖转运蛋白4表达的影响及其机制研究  

Effect of pioglitazone on expressions of adiponectin and glucose transporter 4 in L6 muscle cell and its mechanism

作　　者：戴尧[1] 陈明卫[1] 方朝晖[2] 陈冬[1] 杨宁宁[1] 陈燕[1] 刘剑[2] 王佑民[1] 

机构地区：[1]安徽医科大学第一附属医院内分泌科,合肥230032 [2]安徽中医学院附属医院内分泌科

出　　处：《中华内分泌代谢杂志》2013年第9期812-814,共3页Chinese Journal of Endocrinology and Metabolism

基　　金：国家中医临床研究基地专项课题（JDZX2012005）;安徽省教育厅重点项目（KJ2011A161）

摘　　要：建立棕榈酸诱导的大鼠L6肌细胞胰岛素抵抗模型后，以吡格列酮、c—Jun氨基末端激酶（JNK）抑制剂SP600125、p38丝裂原活化蛋白激酶（p38MAPK）抑制剂SB203580进行干预。应用Western印迹法检测脂联索、葡萄糖转运蛋白4（GLUT4）蛋白表达和JNK、p38MAPK磷酸化水平。结果显示，吡格列酮¨冠著增加胰岛素抵抗状态下I｜6细胞p38MAPK磷酸化、脂联素和GLUT4蛋白表达（P〈0．05或P〈0．01），降低JNK磷酸化水平（P〈0．01）。阻断p38MAPK信号通路后，吡格列酮上调L6细胞GULT4蛋白表达的效应显著降低（P〈0．01），而阻断JNK信号通路却无显著影响（P〉0．05）。After insulin resistance model was induced with palmitate in rat L6 muscle cells, these cells were treated with pioglitazone, a c-Jun-N terminal kinase inhibitor SP600125, and a p38 mitogen-activated protein kinase （p38MAPK） inhibitor SB203580. The adiponectin, glucose transporter 4 （GLUT4） protein expression, and JNK, p38 MAPK phosphorylation levels were determined by Western blot. The results showed that pioglitazone significantly increased p38MAPK phosphorylation, adiponectin and GULT4 protein expression levels （ P〈0. 05 or P〈0.01 ） , and decreased JNK phosphorylation level （ P〈0.01 ）. Pioglitazone-stimulated GLUT4 protein expression was significantly decreased by SB203580（ P〈0.01 ） , not by SP600125.

关 键 词：脂联素 胰岛素抵抗 C-JUN氨基末端激酶 P38丝裂原活化蛋白激酶 吡格列酮 

分 类 号：R587.1[医药卫生—内分泌]