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

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Chongxiao Liu, Liurong Wu, Lihong Fu, Xiaohua Li, Bingxia Zhao, Hongli Zhang
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Abstract

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.

芒果素通过AMPK-mTOR信号通路调节自噬,从而预防葡萄糖脂毒性诱导的胰腺β细胞损伤。
本研究旨在探讨芒果苷(MG)对葡萄糖脂毒性诱导的胰腺β细胞损伤的保护作用。体内给药 MG 能显著降低高脂饮食(HFD)喂养小鼠的血糖水平。MG 可抑制高脂饮食小鼠体内 beta 细胞的凋亡。在体外,MG 可保护 INS-1 细胞免受高糖/棕榈酸(HG/PA)处理后的凋亡和胰岛素分泌损伤。MG 处理可增强自噬通量,而 HG/PA 处理可阻断自噬通量。用 3-甲基腺嘌呤抑制自噬体的形成,或用氯喹阻断自噬体,都会逆转 MG 对 INS-1 细胞的保护作用。MG 处理增加了 AMPK 磷酸化,减少了 INS-1 细胞中 mTOR 的激活。给与 AMPK 阻断剂可抑制 MG 诱导的自噬,在 INS-1 细胞中同时使用 MG 和 mTOR 激活剂也可观察到类似的结果。总之,MG 可通过 AMPK-mTOR 通路调节自噬,从而改善葡萄糖脂毒性诱导的胰岛β细胞损伤。
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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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