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目的 :观察胰淀素对胰岛细胞凋亡和凋亡相关基因表达的影响。方法 :应用放免法检测胰淀素培养后大鼠胰岛细胞和胰岛 β细胞瘤细胞系 (βTc3)高糖刺激后上清液的胰岛素水平 ;应用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记 (TUNEL)技术检测胰淀素培养后大鼠胰岛细胞和小鼠 βTc3细胞凋亡百分率 ;应用定量RT -PCR(QRT -PCR)检测培养后bcl-2、baxmRNA的表达。结果 :胰淀素使原代培养的大鼠胰岛细胞和 βTC3胰岛素分泌功能明显下降 ,使原代培养的大鼠胰岛细胞和 βTC3的凋亡细胞比例明显增加 ;胰岛细胞凋亡过程中 ,诱导凋亡的基因baxmRNA表达水平明显升高 ,抵抗凋亡基因bcl-2mRNA表达水平明显下降。结论 :胰淀素可能通过诱导胰岛细胞凋亡导致或加重糖尿病 ,其中bcl-2/baxmRNA表达比率变化可能起重要作用。
Objective: To observe the effect of amylin on the apoptosis of islet cells and the expression of apoptosis-related genes. Methods: The insulin levels of rat pancreatic islet cells and pancreatic β-cell carcinoma cell line (βTc3) after stimulation with high glucose were detected by radioimmunoassay. Terminal deoxynucleotidyl transferase-mediated dUTP nick end The percentage of apoptosis of pancreatic islet cells and mouse βTc3 cells was detected by TUNEL assay. The expression of bcl-2 and bax mRNA was detected by quantitative RT-PCR (QRT-PCR). Results: Amylin significantly decreased the primary pancreatic islet cells and βTC3 insulin secretion, significantly increased the proportion of primary cultured rat pancreatic islet cells and βTC3 apoptotic cells; during islet cell apoptosis, induced apoptosis The expression of bax mRNA was significantly increased, and the expression of bcl-2 mRNA was significantly decreased. CONCLUSION: Amylin may induce or aggravate diabetes by inducing islet cell apoptosis. The change of bcl-2 / bax mRNA expression may play an important role.