3‑n‑Butylphthalide reduces the oxidative damage of muscles in an experimental autoimmune myositis animal model
- Juan Chen
- Jingyang Wang
- Jiyan Zhang
- Chuanqiang Pu
Affiliations: Department of Neurology, Chinese PLA Medical School, Beijing 100853, P.R. China, Laboratory of Immunology, Academy of Military Medical Sciences, Beijing 100850, P.R. China
- Published online on: July 11, 2017 https://doi.org/10.3892/etm.2017.4766
Copyright: © Chen
et al. This is an open access article distributed under the
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3‑n‑Butylphthalide (NBP) protects the mitochondria and reduces apoptosis in multiple disease models. However, it remains to be determined whether NBP can protect muscle cells from oxidative stress, lipid peroxidation and apoptosis in myositis. In the present study, a myosin immunization protocol was applied to induce experimental autoimmune myositis (EAM) in guinea pigs. After 4 weeks, a low‑ or high‑dose NBP solution was injected intraperitoneally into the guinea pigs, with saline solution serving as the negative control. After 10 days, the guinea pigs were sacrificed and muscle cells were isolated for analysis. The results revealed that NBP increased the superoxide dismutase and catalase activity, and reduced malondialdehyde activity in the EAM model. Furthermore, NBP enhanced ATPase activity in muscle mitochondrial membranes and muscle fiber membranes, reduced the number of apoptotic cells, and differentially regulated the Bcl‑2, Bax and BAD mRNA and protein expression levels in muscle tissues and sera. NBP directly protects muscle mitochondria and muscle cells from oxidative damage. Notably, NBP reduced muscle cell apoptosis. Thus, it is speculated that, as an antioxidant treatment, NBP may benefit individuals with myopathy.