中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2015年
2期
165-168
,共4页
刘丽娟%合湫%苏恒%薛元明%严新民
劉麗娟%閤湫%囌恆%薛元明%嚴新民
류려연%합추%소항%설원명%엄신민
细胞外调节蛋白激酶1/2信号转导通路%βTC-6细胞%糖尿病
細胞外調節蛋白激酶1/2信號轉導通路%βTC-6細胞%糖尿病
세포외조절단백격매1/2신호전도통로%βTC-6세포%당뇨병
Extracellular signal-regulated kinase1/2 (ERK1/2) signal transduction pathway%βTC-6 cell%Diabetes mellitus
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1.38 mmol/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。
目的:探討細胞外調節蛋白激酶(ERK )1/2信號轉導通路在βTC‐6細胞葡萄糖刺激胰島素分泌(GSIS)反應中的作用。方法採用不同濃度葡萄糖刺激βTC‐6細胞,放射免疫法檢測細胞上清液中胰島素濃度,Western blot檢測細胞裂解物ERK1/2燐痠化水平。採用MEK抑製劑 PD98059處理βTC‐6細胞,放射免疫法檢測葡萄糖刺激後上清液中胰島素濃度,Western blot檢測葡萄糖刺激後ERK1/2燐痠化水平。結果βTC‐6細胞在1.38 mmol/L葡萄糖刺激時,胰島素分泌和ERK1/2燐痠化水平達高峰。PD98059可抑製葡萄糖刺激下ERK1/2燐痠化及胰島素分泌,作用與劑量呈正相關。結論ERK1/2信號轉導通路可能在βTC‐6細胞GSIS中髮揮作用。
목적:탐토세포외조절단백격매(ERK )1/2신호전도통로재βTC‐6세포포도당자격이도소분비(GSIS)반응중적작용。방법채용불동농도포도당자격βTC‐6세포,방사면역법검측세포상청액중이도소농도,Western blot검측세포렬해물ERK1/2린산화수평。채용MEK억제제 PD98059처리βTC‐6세포,방사면역법검측포도당자격후상청액중이도소농도,Western blot검측포도당자격후ERK1/2린산화수평。결과βTC‐6세포재1.38 mmol/L포도당자격시,이도소분비화ERK1/2린산화수평체고봉。PD98059가억제포도당자격하ERK1/2린산화급이도소분비,작용여제량정정상관。결론ERK1/2신호전도통로가능재βTC‐6세포GSIS중발휘작용。
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 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 .38 mmol/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 glucose‐stimulated insulin secretion in βTC‐6 cells .