p38 MAPK及其抑制剂在胰岛素调节GLUT4活性中的作用  

Study on the Effects of p38 MAPK and Its Inhibitor on Insulin-regulated GLUT4 Activity

作　　者：李敏[1] 刘琳娟[1] 姚智[1] 牛文彦[1] 

机构地区：[1]天津医科大学免疫学教研室,300070

出　　处：《天津医药》2007年第9期641-643,721,共4页Tianjin Medical Journal

基　　金：国家自然科学基金资助项目(项目编号:30570912);国家自然科学基金委员会(NSFC)-加拿大卫生研究院(CIHR)健康研究合作项目(项目编号:30611120532);天津市应用基础研究重点项目(项目编号:07JCZDJC07900);天津市科技攻关项目(项目编号:06YFG-PSH03300);天津市高等学校科技发展基金项目(项目编号:20040106)

摘　　要：目的:探讨p38丝裂原活化蛋白激酶(p38 MAPK)及其抑制剂SB203580在胰岛素调节葡萄糖转运子4(GLUT4)活性机制中的作用。方法:分别测定胰岛素和SB203580孵育条件下骨骼肌细胞p38 MAPK的磷酸化水平和活性;检测p38 MAPK或SB203580是否与GLUT4直接结合;并测定SB203580对光化学标记细胞膜上的GLUT4的影响。结果:与胰岛素孵育0min时相比,100nmol/L胰岛素使p38 MAPK磷酸化水平增加,最大值为0min时的(2.43±0.21)倍;胰岛素还使p38α和p38βMAPK的活性分别增加了(10.13±0.48)和(7.92±2.17)倍;SB203580可抑制胰岛素的作用;p38 MAPK在体内不与GLUT4直接结合;SB203580仅抑制胰岛素刺激下的GLUT4光化学标记。结论:p38MAPK或SB203580不直接与GLUT4结合;对SB203580敏感的分子参与了胰岛素调节GLUT4活性的作用。Objective： To explore the effects of p38 MAPK and its inhibitor SB203580 on insulin-regulated GLUT4 activity. Methods： p38 MAPK phosphorylation and activity in skeletal muscle cell were measured in insulin and SB203580 treated groups respectively. Combination of p38 MAPK or SB203580 and GLUT4 was detected and the effect of SB203580 on photolabeling GLUT4 on cell membrane was studied. Results： p38 MAPK phosphorylation increased by 100 nmol/L insulin with a maximal value 2.43 ± 0.21 times （insulin treatments 0 min）. The activities of p38 α and p38 β MAPK increased by insulin with （ 10.13 ± 0.48 ） and （7.92 ± 2.17） times respectively. Insulin effect was inhibited by SB203580. p38 MAPK did not bind to GLUT4 directly in vivo. SB203580 only inhibited insuhn-stimulated GLUT4 photolabeling. Conclusion： p38 MAPK and SB203580 do not bind to GLUT4 directly, and S203580-sensitive molecule is involved in the insulin-regulated effect on GLUT4 activity.

关 键 词：丝裂原激活蛋白激酶类 单糖转运蛋白质 类 肌 骨骼 细胞 胰岛素 

分 类 号：R730.264[医药卫生—肿瘤]