APPL1对高糖及炎症因子诱导的胰岛β细胞凋亡和功能损伤的保护作用
The protective effect of APPL1 on high glucose or cytokines-induced pancreatic β-cell apoptosis and dysfunction
目的 明确适配蛋白APPL1在胰岛β细胞中的作用.方法 采用腺病毒转染使INS-1细胞过表达APPL1.Western印迹法检测蛋白表达水平,碘化丙啶/Hoechst染色法检测细胞凋亡,用ELISA检测胰岛素分泌.结果 20 mmol/L葡萄糖或30 U/ml白细胞介素-1β加20 ng/ml TNF-α作用INS-1细胞48h后,可明显诱导胰岛β细胞凋亡(P<0.01),并降低2h葡萄糖刺激的胰岛素分泌水平(P<0.01).INS-1细胞过表达APPL1后,与各自的对照病毒组相比,APPL1可使细胞凋亡降低34.16% ~42.79% (P<0.01),并使葡萄糖刺激的胰岛素分泌升高至对照组的1.39 ~2.20倍(P<0.05).结论 APPL1对高糖和炎症因子诱导的胰岛β细胞损伤具有保护作用,可降低β细胞凋亡并改善葡萄糖刺激的胰岛素分泌.
更多Objective To determine the role of APPL1,an adaptor protein,played in pancreatic β-cell.Methods APPL1 was overexpressed in INS-1 cells with adenovirus encoding APPL1.Western blot was conducted to measure protein cxprcssion.Propidium iodide/Hoechst staining was used to determine the cell apoptosis.Insulin secretion was measured by ELISA.Results Exposure of INS-1 cells to 20 mmol/L glucose or 30U/ml interleukin-1 β plus 20 ng/ml TNF-α 48 h induced β-cell apoptosis (P<0.01) and impaired 2 h glucosestimulated insulin secretion (P< 0.01).Overexpression of APPL1 in INS-1 decreased cell apoptosis by 34.16%-42.79% (P<0.01) and increased glucose-induced insulin secretion by 1.39-2.20 folds compared with control groups (P<0.05).Conclusion APPL1 decreases β-cell apoptosis and increases glucose-stimulated insulin secretion,and thus protects β-cell against high glucose or cytokines-induced dysfunction.
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