细胞外调节蛋白激酶1/2在小鼠胰岛瘤βTC-6细胞胰岛素分泌功能中的作用探讨  

The effect of extracellular signal-regulated kinase 1/2 signal transduction pathway on insulin secretion in βTC-6 cell line

作　　者：刘丽娟[1,2] 合湫 苏恒[1] 薛元明[1] 严新民[3] 

机构地区：[1]云南省第一人民医院内分泌科,昆明650032 [2]武钢总医院干保中心 [3]云南省第一人民医院基础研究所,昆明650032

出　　处：《中国糖尿病杂志》2015年第2期165-168,共4页Chinese Journal of Diabetes

基　　金：云南省自然科学基金面上项目(2005C0002R);云南省中青年学术技术带头人后备人才项目(2007PY01-32)

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,放射免疫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,放射免疫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1.38mmol/L葡萄糖刺激时,胰岛素分泌和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。Objective To investigate the effect of extracellular signal-regulated kinase 1/2（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 insulin was assayed by an insulin RIA kit,and cell lysate was used for protein assay by Western blot.βTC-6 cells were pretreated with MEK inhibitor PD98059 and stimulated with 1.38 mmol/L glucose.And then,supernatants insulin was assayed by Western blot. Results The insulin level and ERK1/2 phosphorylation reach a peak in response to 1.38mmol/L glucose stimulation in βTC-6 cells.MEK inhibitor PD98059 can inhibit insulin secretion and ERK phosphorylation which was induced by glucose stimulation in a dose-dependent manner. Conclusion ERK1/2 signal transduction pathway activation may have an important effect on glucosestimulated insulin secretion in βTC-6 cells.

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 

分 类 号：R736.7[医药卫生—肿瘤]