Baicalin inhibits C2C12 myoblast apoptosis and prevents against skeletal muscle injury

Pan,Yutao; Song,Dongli; Zhou,Weiyan; Lu,Xiuhong; Wang,Haiyan; Li,Zengchun

doi:10.3892/mmr.2019.10298

Baicalin inhibits C2C12 myoblast apoptosis and prevents against skeletal muscle injury

Authors:
- Yutao Pan
- Dongli Song
- Weiyan Zhou
- Xiuhong Lu
- Haiyan Wang
- Zengchun Li
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Affiliations: Department of Emergency and Trauma Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, P.R. China, Zhongshan Hospital Clinical Science Institute, Fudan University, Shanghai 200032, P.R. China, PET Center, Huashan Hospital, Fudan University, Shanghai 200235, P.R. China, Department of Nuclear Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, P.R. China
Published online on: May 27, 2019 https://doi.org/10.3892/mmr.2019.10298
Pages: 709-718

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Abstract

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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