目的：儿童病毒性心肌炎(VMC)发病率高，临床上缺乏有效的治疗药物。该研究旨在探讨黄芪注射液治疗小鼠柯萨奇B3(CVB-3)病毒性心肌炎的疗效及其机制。方法：24只Balb/C鼠腹腔感染柯萨奇病毒B3亲心肌细胞株后，随机等分为两组：黄芪治疗组(黄芪注射液10 g/kg，腹腔注射，每天1次，连续7d)和对照组(同法每天注射等容积注射用水)。实验第8天留取心肌和血液标本，进行心肌病理检查，逆转录多聚酶链反应(RT-PCR)法检测心肌穿孔素(PFP)mRNA表达及放免法检测外周血肿瘤坏死因子-α(TNF-α)水平。结果：①黄芪治疗组心肌组织病理改变明显轻于对照组；②黄芪治疗组心肌PFP mRNA的表达明显低于对照组［(1.10±0.07) vs (1.31±0.12)］(P<0.01)；③黄芪治疗组血清TNF-α含量明显低于对照组［(2.39±0.21) ng/ml vs (2.97±0.32) ng/ml］(P<0.01)。④PFP mRNA表达水平与血清TNF-α含量呈显著正相关(r=0.84，P<0.01)。结论：黄芪注射液对病毒性心肌炎有明显的治疗作用，其机制可能是通过减轻病毒性心肌炎中PFP介导的细胞毒性作用和炎症反应。

OBJECTIVE: Viral myocarditis frequently occurrs in children, but no effective medicines for clinic treatment have been found. This paper aims at studying the effect and mechanism of astragalus injection in the treatment of acute murine myocarditis caused by Coxsackievirus B 3. METHODS: Acute viral myocarditis was induced in 24 Balb/c mice by injection of Coxsackievirus B 3m (CVB 3m ) intraperitoneally. Half of the mice were administered astragalus injection with a dosage of 10 g/kg daily for 7 days (astragalus treated group). The remained received the same amount of normal saline and were used as the control group. On the 8th day after CVB 3m infection, the pathological changes of myocardium were studied. Myocardial perforin expression was detected by reverse transcription polymerase chain reactin (RT PCR) and serum TNF α level was measured by radioimmunoassay. RESULTS: The astragalus treated group showed a significant reduction in myocardial lesions compared with that in the control group. The myocardial perforin expression in the astragalus treated group was much lower than that in the control group [( 1.10 ± 0.07 ) vs ( 1.31 ± 0.12 ); P< 0.01 ]. The serum TNF α level was also significantly lower in the astragalus treated group than that in the control group [( 2.39 ± 0.21 ) vs ( 2.97 ± 0.32 ; P< 0.01 )]. The myocardial perforin expression was significantly positively correlated with the serum TNF α level (r= 0.84 , P< 0.01 ). CONCLUSIONS: Astragalus has protective effects against viral myocarditis by reducing perforin mediated cytotoxicity and inflammatory reaction.