首页|芪骨胶囊含药血清对地塞米松诱导C2C12细胞萎缩的保护作用

芪骨胶囊含药血清对地塞米松诱导C2C12细胞萎缩的保护作用

Protective effects of Qigu Capsule-medicated serum on C2C12 cells atrophy induced by dexamethasone

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目的 观察芪骨胶囊含药血清对地塞米松诱导的C2C12 肌管细胞萎缩的保护作用.方法 制备芪骨胶囊含药血清;体外培养C2C12 细胞,分为正常对照组、地塞米松组、10%空白血清组、10%芪骨胶囊含药血清组,给予相应药物处理 48h后,除正常对照组外再给予 10 μmol/L地塞米松继续培养 24 h,CCK-8 法检测各组细胞活力.用 2%马血清诱导C2C12 细胞分化 6~7 d,按上述分组干预肌管细胞,测量各组肌管细胞直径,Western blot 法检测 MyHC、MuRF-1、Atrogin-1及PI3K/Akt信号通路相关蛋白表达.加入 PI3K 抑制剂 LY294002,测量肌管细胞直径,检测MuRF-1、Atorgin-1、PI3K/Akt信号通路相关蛋白表达.结果 与正常对照组比较,地塞米松组及空白血清组C2C12细胞活力降低(P<0.01),肌管细胞直径减少(P<0.01),MuRF-1、Atrogin-1 蛋白表达升高(P<0.01),MyHC蛋白表达及PI3K、Akt、mTOR、FoxO3a磷酸化水平降低(P<0.01);与地塞米松组比较,芪骨胶囊含药血清组细胞活力升高(P<0.01),肌管细胞直径增加(P<0.01),MuRF-1、Atrogin-1 蛋白表达降低(P<0.01),MyHC蛋白表达及PI3K、Akt、mTOR、FoxO3a的磷酸化水平升高(P<0.05,P<0.01).芪骨胶囊含药血清联合LY294002 干预后,芪骨胶囊含药血清的抗肌管萎缩效应消失(P<0.01),MuRF-1、Atorgin-1 蛋白表达升高(P<0.01),而 PI3K、Akt、mTOR、FoxO3a磷酸化水平降低(P<0.05,P<0.01).结论 芪骨胶囊含药血清能减轻地塞米松诱导的C2C12 肌管细胞萎缩,其机制可能与激活PI3K/Akt信号通路相关.
AIM To observe the protective effects of Qigu Capsule-medicated serum on C2C12 myotube cell atrophy induced by dexamethasone.METHODS The Qigu Capsule-medicated serum was prepared.C2C12 cells cultured in vitro were divided into the normal control group,the dexamethasone group,the 10%blank serum group and the 10%Qigu Capsule-medicated serum group for 48 h,corresponding drug treatment,followed by 24 h culture with 10 μmol/L dexamethasone except the control group,and had cell viability detection by CCK-8 method.With their myotube cells intervened accordingly by the aforementioned regime following 6-7 days differentiation with 2%horse serum induction,the C2C12 cells had their myotube cells diameter measured;and the expressions of proteins related to MyHC,MuRF-1,Atrogin-1 and PI3K/Akt signaling pathway detected by Western blot.The impact of PI3K inhibitor LY294002 on the diameter of myotube cells and the expression of MuRF-1,Atorgin-1 and PI3K/Akt signaling pathway related proteins were detected as well.RESULTS Compared with the normal control group,the dexamethasone group and the blank serum group were observed with decreased viability of C2C12 cells(P<0.01),decreased diameter of myotube cells(P<0.01),increased protein expressions of MuRF-1 and Atrogin-1(P<0.01),and decreased expression of MyHC protein and phosphorylation levels of PI3K,Akt,mTOR and FoxO3a(P<0.01).Compared with the dexamethasone group,the Qigu Capsule-medicated serum group showed increased viability of C2C12 cells(P<0.01);increased diameter of myotube cells(P<0.01);decreased protein expressions of MuRF-1 and Atrogin-1(P<0.01);and increased expression of MyHC protein and phosphorylation levels of PI3K,Akt,mTOR and FoxO3a(P<0.05,P<0.01).The intervention of LY294002 upon the Qigu Capsule-medicated serum group offset the anti-muscular tube atrophy effect(P<0.01),increased the protein expressions of MuRF-1 and Atorgin-1(P<0.01),and decreased the phosphorylation levels of PI3K,Akt,mTOR and FoxO3a(P<0.05,P<0.01).CONCLUSION The Qigu Capsule-medicated serum can alleviate the atrophy of C2C12 myotubes induced by dexamethasone,and its mechanism may be related to the activation of PI3K/Akt signaling pathway.

Qigu CapsuleC2C12 myoblastscell atrophyPI3K/Akt signaling pathway

石金玉、杨宗睿、葛海雅、郭海玲、詹红生

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上海中医药大学附属曙光医院石氏伤科医学中心,上海 200120

上海市中医药研究院骨伤科研究所,上海 200120

芪骨胶囊 C2C12成肌细胞 细胞萎缩 PI3K/Akt信号通路

国家中医药管理局项目(2019)上海市科学技术委员会项目上海市卫生健康委员会项目上海市中医药发展办公室项目上海市申康医院发展中心项目上海中医药大学项目(2018)

20MC1920600shslczdzk03901ZY2018-2020-CCCX-1010SHDC2020CR3090B

2023

中成药
国家食品药品监督管理局,信息中心中成药信息站,上海中药行业协会

中成药

CSTPCDCSCD北大核心
影响因子:1.217
ISSN:1001-1528
年,卷(期):2023.45(12)
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