来自:中国糖尿病杂志 编辑:刘丽娟 合湫 苏恒 薛元明 严新民|点击数:|2015-02-06
糖尿病基础研究
【摘要】 目的 探讨细胞外调节蛋白激酶(ERK)1/2信号转导通路在βTC-6细胞葡萄糖刺激胰岛素分泌(GSIS)反应中的作用。 方法 采用不同浓度葡萄糖刺激βTC-6细胞,放免法检测细胞上清液中胰岛素浓度,Western blot检测细胞裂解物ERK1/2磷酸化水平。采用MEK抑制剂PD98059处理βTC-6细胞,放免法检测葡萄糖刺激后上清液中胰岛素浓度,Western blot检测葡萄糖刺激后ERK1/2磷酸化水平。 结果 βTC-6细胞在1.38 mmol/L葡萄糖刺激时胰岛素分泌达高峰,ERK1/2磷酸化水平达高峰。PD98059可抑制葡萄糖刺激下ERK1/2磷酸化及胰岛素分泌,作用与剂量呈正相关。 结论 ERK1/2信号转导通路可能在βTC-6细胞GSIS中发挥作用。
【关键词】细胞外调节蛋白激酶1/2信号转导通路;βTC-6细胞;糖尿病
【Abstract】 Objective To investigate the effect of extracellular signal-regulated kinase1/2 (ERK1/2) signal transduction pathway on glucose stimulated insulin secretion in βTC-6 cell line. Methods βTC-6 cells were stimulated with different concentration of glucose. Supernatants were collected for insulin assays by an insulin RIA kit, cell lysate was used for Western blotting.βTC-6 cells were pretreated with MEK inhibitor PD98059 and stimulated with 1.38 mmol/L glucose. Supernatants were collected for insulin assays, cell lysate was used for Western blotting. Results The insulin level and ERK1/2 phosphorylation reach a peak in response to 1.38 mM glucose stimulation in βTC-6 cells. MEK inhibitor PD98059 can inhibit insulin secretion and ERK phosphorylation induced by glucose stimulation in a dose-dependent manner. Conclusion ERK1/2 signal transduction pathway activation may have an important effect on glucose stimulated insulin secretion in βTC-6 cells.
【Key words】Extracellular signal-regulated kinase1/2 (ERK1/2) signal transduction pathway;βTC-6 cell;Diabetes mellitus
版权所有:《中国糖尿病杂志》社 主管单位:中华人民共和国教育部 主办单位:北京大学
地址:北京市西城区大红罗厂街1号 邮编:100034 电话(传真):010-88505683
中国糖尿病杂志社版权所 京ICP备11029051号-1 Powered by JiuduCMS 技术支持:九度创想