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Metformin inhibits Aβ 25‐35 ‐induced apoptotic cell death in SH‐SY5Y cells
Author(s) -
Li LiXia,
Liu MengYu,
Jiang Xue,
Xia ZhenHong,
Wang YuXiang,
An Di,
Wang HongGang,
Heng Bin,
Liu YanQiang
Publication year - 2019
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13279
Subject(s) - metformin , sh sy5y , autophagy , intracellular , apoptosis , programmed cell death , neurotoxicity , extracellular , neuroprotection , microbiology and biotechnology , pharmacology , chemistry , cell culture , biology , medicine , endocrinology , biochemistry , diabetes mellitus , toxicity , genetics , neuroblastoma
Metformin, a first‐line drug for type‐2 diabetes, plays a potentially protective role in preventing Alzheimer's disease (AD), but its underlying mechanism is unclear. In this study, Aβ 25‐35 ‐treated SH‐SY5Y cells were used as a cell model of AD to investigate the neuroprotective effect of metformin, as well as its underlying mechanisms. We found that metformin decreased the cell apoptosis rate and death, ratio of Bcl‐2/Bax, and expression of NR2A and NR2B, and increased the expression of LC3 in Aβ 25‐35 ‐treated SH‐SY5Y cells. Metformin also reduced intracellular and extracellular Glu concentrations, as well as the intracellular concentration of Ca 2+ and ROS in Aβ 25‐35 ‐treated SH‐SY5Y cells. These findings suggest that metformin inhibits Aβ 25‐35 ‐treated SH‐SY5Y cell death by inhibiting apoptosis, decreasing intracellular Ca 2+ and ROS by reducing neurotoxicity of excitatory amino acids, and by possibly reversing autophagy disorder via regulating autophagy process.