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目的探讨氧化苦参碱(oxymatrine,OMT)对病毒性心肌炎小鼠心肌细胞凋亡及其凋亡相关因子蛋白表达的影响。方法 42只BALB/c小鼠随机分为正常对照组(NC)、病毒性心肌炎模型组(VM)、OMT高剂量组(OMT-H,25 mg·kg~(-1)·d~(-1))、OMT中剂量组(OMT-M,12.5 mg·kg~(-1)·d~(-1))、OMT低剂量组(OMT-L,6.25 mg·kg~(-1)·d~(-1))、OMT极低剂量组(OMT-EL,3.125 mg·kg~(-1)·d~(-1))、利巴韦林对照组(RB,100 mg·kg~(-1)·d~(-1))。病毒性心肌炎小鼠由柯萨奇病毒B3型腹腔注射感染所致,各治疗组从末次给予病毒24 h后开始,腹腔注射,每日1次。于治疗第12天,每组处死小鼠6只,留取心肌标本。TUNEL法检测心肌细胞凋亡情况,免疫印迹法和免疫组织化学法检测Bcl-2和Bax蛋白的表达情况。结果 OMT治疗显著降低了病毒性心肌炎小鼠凋亡心肌细胞的数量,与病毒性心肌炎模型组比较,OMT-L组效果最佳(P<0.01)。与病毒性心肌炎模型组小鼠比较,OMT治疗组的小鼠心肌组织中Bax蛋白表达降低,而Bcl-2蛋白表达没有明显改变。结论氧化苦参碱可减少病毒性心肌炎小鼠心肌细胞的凋亡,该作用与下调Bax蛋白表达有关。
Objective To investigate the effect of oxymatrine (OMT) on the apoptosis of cardiomyocytes and the expression of apoptosis related protein in myocardium of mice with viral myocarditis. Methods 42 BALB / c mice were randomly divided into normal control group (NC), viral myocarditis model group (VM) and OMT high dose group (OMT-H, 25 mg · kg -1 · d ~ (OMT-M, 12.5 mg · kg -1 · d -1), OMT low dose group (OMT-L, 6.25 mg · kg -1) (OMT-EL, 3.125 mg · kg -1 · d -1), ribavirin control group (RB, 100 mg · kg -1 · d -1) (-1) · d -1). Viral myocarditis in mice caused by intraperitoneal injection of Coxsackie virus B3 infection, each treatment group from the last virus after 24 h, intraperitoneal injection, once daily. On the 12th day of treatment, 6 mice in each group were sacrificed, and the myocardial samples were collected. The apoptosis of cardiomyocytes was detected by TUNEL method. The expressions of Bcl-2 and Bax protein were detected by Western blotting and immunohistochemistry. Results OMT treatment significantly reduced the number of apoptotic cardiomyocytes in viral myocarditis mice. Compared with the viral myocarditis model group, OMT-L group had the best effect (P <0.01). Compared with the mice in viral myocarditis model group, the expression of Bax protein in the myocardium of OMT group was decreased, while the expression of Bcl-2 protein did not change significantly. Conclusion Oxymatrine can reduce the cardiomyocyte apoptosis in viral myocarditis mice, which may be related to the down-regulation of Bax protein expression.