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目的:探讨胰高血糖素样肽-1(GLP-1)对内质网应激诱导的胰岛β细胞系INS-1细胞凋亡的影响及其机制。方法:培养INS-1细胞,接种后分组:正常对照组、0.1μM毒胡萝卜素(TG)处理组、0.5μM TG处理组、1μM TG处理组、GLP-1(10n M)处理组、TG+GLP-1处理组、SB415286(10μM)处理组和TG+SB415286处理组。细胞处理后,TUNEL染色法检测细胞凋亡,Western blot检测蛋白表达水平。结果:与正常对照组相比,TG组INS-1细胞凋亡率均显著升高(P<0.05,P<0.01),随着TG浓度的增加Caspase-3活性逐渐升高。与TG处理组相比,TG和GLP-1共同处理组INS-1细胞凋亡率显著下降(P<0.01),且Caspase-3活性下降;TG和GLP-1共同处理组糖原合成酶激酶-3β(GSK-3β)的活性下降。TG和SB415286共同处理组INS-1细胞凋亡率显著下降(P<0.05),且Caspase-3活性下降。结论 :GLP-1可以通过抑制GSK-3β活性减轻内质网应激引起的损伤从而保护β细胞。
AIM: To investigate the effect and mechanism of glucagon-like peptide-1 (GLP-1) on apoptosis induced by endoplasmic reticulum stress-induced pancreatic β-cell line INS-1 cells. Methods: INS-1 cells were cultured and inoculated into the normal control group, 0.1μM thapsigargin (TG) group, 0.5μM TG treatment group, 1μM TG treatment group, GLP- GLP-1 treatment group, SB415286 (10 μM) treatment group and TG + SB415286 treatment group. After the cells were treated, the apoptosis was detected by TUNEL staining and the protein expression was detected by Western blot. Results: Compared with the normal control group, the apoptosis rate of INS-1 cells in TG group was significantly increased (P <0.05, P <0.01). Caspase-3 activity increased gradually with the increase of TG concentration. Compared with TG treatment group, the apoptosis rate of INS-1 cells was significantly decreased (P <0.01) and the activity of Caspase-3 was decreased in TG and GLP-1 co-treatment group; TG and GLP-1 co-treatment group glycogen synthase kinase -3β (GSK-3β) activity decreased. The apoptosis rate of INS-1 cells was significantly decreased (P <0.05) and the activity of Caspase-3 was decreased in TG and SB415286 co-treated groups. Conclusion: GLP-1 can protect the β cells by inhibiting GSK-3β activity and alleviating endoplasmic reticulum stress-induced injury.