Resveratrol Reverses Myogenic Induction Suppression Caused by High Glucose Through Activating the SIRT1/AKT/FOXO1 Pathway

被引:0
作者
Liu, Meiling [1 ]
Cheng, Luyang [1 ]
Li, Xianglu [1 ]
Wang, Hongzhi [1 ]
Wang, Manfeng [1 ]
Gan, Lu [1 ,2 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 2, Dept Geriatr, Harbin, Peoples R China
[2] Harbin Med Univ, Affiliated Hosp 2, Dept Geriatr, 246 Xuefu Rd, Harbin 150086, Peoples R China
关键词
Resveratrol; bone marrow mesenchymal stem cells; myogenic induction; AKT; FOXO1; MESENCHYMAL STEM-CELLS; DIFFERENTIATION; MUSCLE; APOPTOSIS; FRAILTY;
D O I
10.1177/1934578X231159722
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
BackgroundDifferentiated bone marrow mesenchymal stem cells (BMSCs) may be a therapeutic strategy to treat sarcopenia caused by high glucose. The effects of resveratrol in the myogenic induction of BMSCs under high glucose are unknown. We evaluated the effects and possible mechanisms of high glucose and resveratrol on myogenic induction of rat BMSCs. MethodsPrimary rat BMSCs were isolated and purified from Sprague-Dawley rats aged between 3 and 4 weeks. Rat BMSCs were differentiated into myogenic cells using conditioned medium and treated with glucose and/or resveratrol along with EX527 (a specific silent information regulator 1 [SIRT1] inhibitor). The expressions of MyoD1 and Myogenin were measured. The reactive oxygen species (ROS) level, superoxide dismutase (SOD) activity, and the expressions of FOXO1 and p-AKT/AKT during myogenic induction were also examined. ResultsHigh glucose decreased cell viability, cell proliferation, and SOD activity, increased intracellular ROS levels, and inhibited the AKT/FOXO1. Resveratrol reversed myogenic induction suppression caused by high glucose, partly through restoring cell proliferation and viability, reducing peroxidative damage, and activating the AKT/FOXO1 pathway; this effect was eliminated by EX527. ConclusionOur results indicate that resveratrol promoted myogenic induction and partially reversed the suppression of myogenic induction caused by high glucose through activating the SIRT1/AKT/FOXO1 pathway.
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页数:11
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