氧化苦参碱对病毒性心肌炎小鼠心肌细胞凋亡及相关因子的影响

Effect of OMT on Apoptosis and Its Protein Bcl-2 and Bax of Myocardium in Mice with Viral Myocarditis

关键词:  氧化苦参碱  病毒性心肌炎  柯萨奇病毒B3型  细胞凋亡

Key words:  oxymatrine(OMT)  viral myocarditis  coxsackievirus B3(CVB3)  apoptosis

摘要:

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。

Abstract:

OBJECTIVE To investigated the effect of oxymatrine(OMT) on apoptosis and its protein Bcl-2 and Bax of myocardium in mice with viral myocarditis. METHODS BALB/c mice were used and inoculated intraperitoneally with CVB3. Twenty-four hours after the last inoculation with CVB3, the infected mice were intraperitoneally injected with OMT or ribavirin. The mice were divided into normal control group(NC), viral myocarditis model group(VM), OMT high, middle, low and extreme low group(OMT-H, OMT-M, OMT-L, OMT-EL. the dose were 25, 12.5, 6.25, 3.125 mg·kg^-1·d^-1, respectively.)and ribavirin group(RB, 100 mg·kg^-1·day^-1). six mice from each group were sacrificed and their myocardial tissues were obtained after 12 d. The myocardial cells apoptosis were detected through TUNEL assay, and the protein expression of Bcl-2 and Bax were detected using western blot and immunohistochemical method. RESULTS OMT induced myocardial cells apoptosis in viral myocarditis mice, compared with VM, the effect of OMT-L was remarkable (P<0.01). The protein expression of Bax was decreased in OMT treatment groups, but the protein expression of Bcl-2 was unchanged after OMT treatment. CONCLUSION OMT may reduce myocardial cells apoptosis in viral myocarditis mice, and it is related to regulating Bax protein in vivo.