基础医学与临床2026，Vol.46Issue(1)：56-62,7.DOI:10.16352/j.issn.1001-6325.2026.01.0056
灰树花多糖改善地塞米松诱导的小鼠骨骼肌细胞系C2C12模型肌管的萎缩
Grifola frondosa polysaccharide improves dexamethasone induced atrophy of myotube models from mouse skeletal muscle cell line C2C12
摘要
Abstract
Objective To investigate the mechanism by which Grifola frondosa polysaccharide(GFP)mitigates dexamethasone(DEX)-induced atrophy of myotubes in mouse skeletal muscle cell line C2C12(C2C12 myotube).Methods C2C12 cells were divided into normal group(NOR),dexamethasone group(DEX),low-dose GFP(GFP-L),medium-dose GFP(GFP-M)and high-dose GFP-H intervention DEX groups(concentrations of 20,50,and 100 μg/mL,respectively).Immunofluorescence microscopy and Western blot were employed to assess my-osin heavy chain(MyHC)expression.Western blot and RT-qPCR were utilized to evaluate the protein and mRNA levels of muscle-specific ring finger protein 1(MuRF1),muscle atrophy F-box protein(Atrogin1)as well as phosphorylation of AMPK and forkhead box protein O3(FOXO3a).The expression of SIRT1.ATP and mitochon-drial protein content were measured with commercially available kits.Results GFP-M and GFP-H groups signifi-cantly increased myotube length,fusion index and MyHC expression in DEX-treated cells(P＜0.05).Additionally,GFP treatment markedly down-regulated the protein and mRNA expression level of Atrogin1,MuRF1 and Myostatin(P＜0.05).The phosphorylation level of AMPK and FOXO3a and the expression of SIRT1 were also significantly reduced(P＜0.05).The SIRT1 inhibitor-induced aberrant expression of FOXO3a,Atrogin1,and MuRF1 was effec-tively reversed by GFP.Conclusions Grifola frondosa polysaccharide may alleviate DEX-induced atrophy of C2C12 myotubes through a SIRT1-mediated AMPK/FOXO3a signaling pathway.关键词
灰树花多糖/肌肉萎缩/地塞米松/AMPK/FOXO3a信号通路Key words
Grifola frondosa polysaccharide/muscle atrophy/dexamethasone/AMPK/FOXO3a signaling pathway分类
医药卫生引用本文复制引用
张兆波,张文岭,赵飞飞,杜国涛..灰树花多糖改善地塞米松诱导的小鼠骨骼肌细胞系C2C12模型肌管的萎缩[J].基础医学与临床,2026,46(1):56-62,7.基金项目
河北省中医药管理局项目(2020525) （2020525）
