自噬在他汀致胰岛细胞分泌功能障碍的作用  

Role of autophagy in the paracrisis of insulin of islet cells after intervention of statins

作　　者：安丽[1] 朱孔博[1] 钱玲林 林燕珊[1] 任利群[1] 

机构地区：[1]东南大学附属中大医院老年医学科,江苏南京210009

出　　处：《现代医学》2017年第8期1064-1066,共3页Modern Medical Journal

基　　金：江苏省自然科学基金资助项目(BK20141345)

摘　　要：目的:探讨自噬在他汀致胰岛细胞分泌障碍中的作用。方法:将INS-1细胞用不同浓度阿托伐他汀钙(0.2μmol·L^(-1)、2μmol·L^(-1)、20μmol·L^(-1))干预24 h,采用钾离子刺激胰岛素分泌的方法来检验INS-1细胞的分泌功能,ELISA方法检测胰岛素浓度,Western blotting检测自噬相关蛋白Beclin 1、LC3 Ⅱ蛋白水平。结果:阿托伐他汀钙干预24 h后,INS-1细胞胰岛素分泌功能被抑制,其抑制作用随阿托伐他汀钙浓度增加而增加,自噬相关蛋白Beclin 1、LC3 Ⅱ表达上调。结论:阿托伐他汀钙以浓度依赖性地抑制INS-1细胞的胰岛素分泌,自噬可能参与了阿托伐他汀钙致INS-1细胞分泌障碍。Objective： To investigate the impact of autophagy in the paracrisis of insulin of INS-l cells after intervention of atorvastatin calcium. Methods： After intervention of atorvastatin calcium（ 0. 2 μmol · L^（-1）,2 μmol·L^（-1）,20 μmol·L^（-1）） for 24 h,potassium chloride was used to test insulin secretion function of INS-1 cells,ELISA was used to detect insulin concentration,Beclin 1 and LC3 protein levels were tested by Western blotting. Results：24 h after atorvastatin intervention,insulin secretion function of INS-1 cells was inhibited along with the increased concentration of atorvastatin calcium,further more,protein levels of Beclin 1 and LC3 Ⅱ were up-regulated. Conclusion： Atorvastatin inhibited insulin secretion in INS-1 cells in a concentration-dependent manner along with increased levels of protein relating to the of activation of autophagy,suggesting that autophagy is involved in the molecular mechanisms of atorvastatin leading to the paracrisis of insulin of INS-1 cells.

关 键 词：阿托伐他汀 自噬 BECLIN 1 LC3 Ⅱ INS-1细胞 

分 类 号：R587.1[医药卫生—内分泌]