Chen Juan, Wang Jingyang, Zhang Jiyan, Pu Chuanqiang
Department of Neurology, Chinese PLA Medical School, Beijing 100853, P.R. China.
Department of Neurology, The 309th Hospital of PLA, Beijing 100091, P.R. China.
Exp Ther Med. 2017 Sep;14(3):2085-2093. doi: 10.3892/etm.2017.4766. Epub 2017 Jul 11.
3--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.
3-丁基苯酞（NBP）在多种疾病模型中可保护线粒体并减少细胞凋亡。然而，NBP是否能保护肌炎中的肌肉细胞免受氧化应激、脂质过氧化和细胞凋亡的影响仍有待确定。在本研究中，采用肌球蛋白免疫方案诱导豚鼠实验性自身免疫性肌炎（EAM）。4周后，将低剂量或高剂量的NBP溶液腹腔注射到豚鼠体内，以生理盐水作为阴性对照。10天后，处死豚鼠并分离肌肉细胞进行分析。结果显示，在EAM模型中，NBP提高了超氧化物歧化酶和过氧化氢酶活性，降低了丙二醛活性。此外，NBP增强了肌肉线粒体膜和肌纤维膜中的ATP酶活性，减少了凋亡细胞数量，并差异调节了肌肉组织和血清中Bcl-2、Bax和BAD的mRNA及蛋白表达水平。NBP直接保护肌肉线粒体和肌肉细胞免受氧化损伤。值得注意的是，NBP减少了肌肉细胞凋亡。因此，推测作为一种抗氧化治疗方法，NBP可能对患有肌病的个体有益。
