Mangiferin prevents glucolipotoxicity-induced pancreatic beta-cell injury through modulation of autophagy via AMPK-mTOR signaling pathway

被引:0
|
作者
Liu, Chongxiao [1 ]
Wu, Liurong [1 ]
Fu, Lihong [1 ]
Li, Xiaohua [1 ]
Zhao, Bingxia [2 ]
Zhang, Hongli [1 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Dept Endocrinol, Peoples Hosp 7, Shanghai, Peoples R China
[2] Tongji Univ, Shanghai Peoples Hosp 10, Ctr Minimally Invas Treatment Tumor, Dept Med Ultrasound,Sch Med, Shanghai, Peoples R China
关键词
Mangiferin; pancreatic beta-cell; autophagy; AMPK; glucolipotoxicity; INHIBITION; ACTIVATION; STRESS; LEADS; MASS;
D O I
10.1080/13813455.2024.2387697
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of this study was to investigate the protective effects of Mangiferin (MG) on glucolipotoxicity-induced pancreatic beta-cell injury. In vivo administration of MG significantly reduced the level of blood glucose in high-fat diet (HFD)-fed mice. MG treatment inhibited beta-cell apoptosis in HFD-treated mice. In vitro, MG protected INS-1 cells against apoptosis and impairment of insulin secretion following High glucose/Palmitic acid (HG/PA) treatment. MG treatment enhanced autophagy flux which was blocked by HG/PA treatment. Inhibition of autophagosome formation by 3-Methyladenine or blockade of autolysosome by Chloroquine reversed the protective effects of MG on INS-1 cells. MG treatment increased AMPK phosphorylation and reduced mTOR activation in INS-1 cells. Administration of the AMPK blocker abrogated MG-induced autophagy, and similar results were observed in INS-1 cells after cotreatment with MG and mTOR activator. In conclusion, MG ameliorated pancreatic beta-cell injury induced by glucolipotoxicity through modulation of autophagy via the AMPK-mTOR pathway.
引用
收藏
页码:71 / 80
页数:10
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