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目的:观察曲美他嗪对M株柯萨奇病毒B3(CVB3m)感染的病毒性心肌炎小鼠的保护作用并探讨其可能作用机制。方法:以CVB3m诱导的病毒性心肌炎Balb/c小鼠模型为研究对象。201只清洁级近交系4～6周龄雄性Balb/c小鼠随机分成5组。正常对照小鼠20只(正常组);病毒性心肌炎小鼠55只(心肌炎组);喂养曲美他嗪10 mg/(kg.d)的正常小鼠20只(药物对照组);喂养曲美他嗪10 mg/(kg.d)的病毒性心肌炎小鼠53只(低剂量治疗组);喂养曲美他嗪20 mg/(kg.d)的病毒性心肌炎小鼠53只(高剂量治疗组)。观察各组血清中肌钙蛋白I(cTnI)水平、血清中超氧化物歧化酶(SOD)、丙二醛(MDA)含量的变化以及心肌组织中Fas mRNA表达水平的变化。结果:小鼠感染CVB3m后第7天及第14天,与正常组及药物对照组比较,心肌炎组、低剂量治疗组和高剂量治疗组血清cTnI水平、MDA含量显著升高,SOD含量显著降低,Fas mRNA的表达显著增加,差异有统计学意义(P<0.05)。小鼠感染CVB3m后第7天,与心肌炎组比较,低剂量治疗组和高剂量治疗组血清cTnI水平显著降低,MDA含量显著降低,差异有统计学意义(P<0.05),与心肌炎组及低剂量组比较,高剂量治疗组SOD含量显著升高,Fas mRNA的表达显著减少,差异有统计学意义(P<0.05)。感染CVB3m后第14天,与心肌炎组比较,低剂量治疗组和高剂量治疗组血清cTnI水平、MDA含量显著降低,SOD含量显著升高,Fas mRNA的表达显著减少,差异有统计学意义(P<0.05),与低剂量治疗组比较,高剂量治疗组上述指标变化更明显,差异有统计学意义(P<0.05)。结论:曲美他嗪能够减少病毒性心肌炎中心肌细胞的损害。其机制可能与其抗氧化作用以及通过下调Fas mRNA水平抑制心肌细胞凋亡有关。
Objective: To observe the protective effect of trimetazidine on mice with viral myocarditis infected with C strain of Coxsackievirus B3 (CVB3m) and to explore its possible mechanism. Methods: The Balb / c mouse model of viral myocarditis induced by CVB3m was studied. 201 clean-grade inbred lines 4 to 6-week-old male Balb / c mice were randomly divided into five groups. 20 normal mice (normal group), 55 mice with viral myocarditis (myocarditis group), 20 mice (drug control group) fed trimetazidine 10 mg / (kg · d) Fifty-three mice with viral myocarditis at the dose of 10 mg / (kg.d) of meridalizine (low-dose treatment group) and 53 mice with viral myocarditis fed trimetazidine 20 mg / (kg.d) therapy group). Serum levels of troponin I (cTnI), changes of serum superoxide dismutase (SOD), malondialdehyde (MDA) and the expression of Fas mRNA in myocardium were observed. Results: On the 7th day and the 14th day after CVB3m infection, compared with the normal group and the drug control group, the level of cTnI, the content of MDA and the level of SOD in the myocarditis group, the low-dose treatment group and the high-dose treatment group were significantly decreased , Fas mRNA expression increased significantly, the difference was statistically significant (P <0.05). On the 7th day after CVB3m infection, compared with the myocarditis group, the levels of cTnI and the content of MDA in the low-dose and high-dose treatment groups were significantly decreased (P <0.05) Compared with the dose group, the SOD level in the high-dose treatment group was significantly increased, and the expression of Fas mRNA was significantly decreased (P <0.05). On the 14th day after CVB3m infection, compared with the myocarditis group, the levels of cTnI, the content of MDA and the content of SOD in the low-dose group and the high-dose group were significantly decreased, while the expression of Fas mRNA was significantly decreased (P <0.05). Compared with the low-dose treatment group, the above-mentioned indicators of the high-dose treatment group changed more obviously, the difference was statistically significant (P <0.05). Conclusion: Trimetazidine can reduce the damage of cardiomyocytes in viral myocarditis. The mechanism may be related to its anti-oxidative effects and the inhibition of cardiomyocyte apoptosis by down-regulating Fas mRNA levels.