肌发生
细胞生物学
肌生成素
MyoD公司
蛋白激酶B
细胞
生物
分子生物学
免疫印迹
细胞周期
作者
Yu Tao Pan,Dongli Song,Weiyan Zhou,Xiuhong Lu,Haiyan Wang,Zengchun Li
出处
期刊:Molecular Medicine Reports
[Spandidos Publications]
日期:2019-07-01
卷期号:20 (1): 709-718
被引量:3
标识
DOI:10.3892/mmr.2019.10298
摘要
Anti‑apoptotic and anti‑inflammatory treatments are imperative for skeletal muscle regeneration following injury. Baicalin is well known and has previously been investigated for its role in the treatment of injury and inflammatory diseases. Therefore, the present study aimed to investigate the effects of baicalin in inhibiting apoptosis of C2C12 myoblasts and preventing skeletal muscle injury. A cell counting kit‑8 (CCK‑8) assay and Annexin V/PI staining were initially performed to measure cell viability and apoptosis under conditions of H2O2 exposure with or without baicalin. Subsequently, oxidative activity, mitochondrial function, mitochondrial apoptogenic factors and caspase proteins were analyzed to examine the mechanism underlying the effect of baicalin on inhibiting apoptosis in C2C12 myoblasts. Furthermore, BALB/C mice with skeletal muscle injuries were established, and the potential application of baicalin for anti‑apoptotic and anti‑inflammatory effects was examined via small animal β‑2‑[18F]‑fluoro‑2‑deoxy‑D‑glucose (18F‑FDG) positron emission tomography (PET) imaging and pathological examination. The CCK‑8 assay and Annexin V/PI staining revealed cell death in the C2C12 myoblasts induced by H2O2, which was apoptotic, and this was effectively reversed by treatment with baicalin. H2O2 increased the reactive oxygen species and malondialdehyde levels in C2C12 myoblasts, which was caused by mitochondrial dysfunction, decreased expression of cytochrome c and apoptosis‑inducing factor from cytosolic and mitochondrial fractions, and activated expression of caspase‑3 and caspase‑9; however, treatment with baicalin reversed these effects. In addition, small animal PET imaging revealed that treatment with baicalin decreased the accumulation of FDG by ~65.9% in the injured skeletal muscle induced by H2O2. These pathological results also confirmed the protective effect of baicalin on injured skeletal muscle. Taken together, the results of the present study indicated that baicalin effectively inhibited the apoptosis of C2C12 myoblasts and protected skeletal muscle from injury, which may have potential therapeutic benefits for patients in a clinical setting.
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