目的 研究牛磺酸(taurine，Tau) 对柯萨奇病毒B₃及多柔比星(ADR)所致心肌炎后心肌纤维化的抑制作用并探讨其机制。方法 ①以柯萨奇病毒B₃建立小鼠病毒性心肌炎模型，分为正常对照组、病毒性心肌炎模型组及Tau治疗组(1 000、500和250 mg·kg-1·d-1)，测定小鼠血清中乳酸脱氢酶（LDH)、天冬氨酸氨基转移酶（AST）、肌酸激酶同工酶MB（CK-MB）的含量及超氧化物歧化酶（SOD）的活性，电镜观察心肌超微结构的变化。②以ADR建立大鼠心肌炎模型，将实验动物分为模型组及Tau 治疗组(400、200、100 mg·kg-1·d-1) ，检测大鼠血清中LDH、AST、肌酸激酶（CK）、丙二醛（MDA）的含量及SOD的活性变化；ELISA 法测定大鼠血清中转化生长因子β₁ (TGF-β₁ )及肿瘤坏死因子α(TNF-α)的含量；HE染色观察各组心肌组织的改变。 结果 ①柯萨奇病毒B₃可导致小鼠心肌细胞损伤，模型组血清中LDH、AST、CK-MB的含量增高、SOD的活性降低，而Tau各剂量治疗组均可降低LDH、AST、CK-MB的含量（P<0.05或P<0.01），Tau治疗组(1 000、500 mg·kg-1·d-1)可增强SOD的活性（P<0.05或P<0.01）；电镜显示模型组肌节紊乱、断裂、溶解，肌丝部分溶解，肌膜破损，心肌细胞排列混乱，Tau治疗组心肌组织损伤程度得到改善。②大鼠心肌炎Tau (400、200 mg·kg-1·d-1)治疗组的LDH、AST 、CK及MDA的含量明显降低，SOD活性增强，Tau (400、200、100 mg·kg-1·d-1)治疗组TGF-β₁及TNF-α含量均降低，与模型组比较具有统计学差异（P<0.05或P<0.01）；HE 染色显示，ADR模型组心肌纤维增生，排列紊乱，肌浆肿胀，细胞内水肿，线粒体结构损害，Tau 明显减轻ADR所引起的心肌损伤。结论 Tau 可通过抗脂质过氧化作用，对柯萨奇病毒B₃、ADR所致心肌炎发挥保护作用，并抑制TGF-β₁及TNF-α的表达，降低ADR心肌炎继发的心肌纤维化的发生。

OBJECTIVE To investigate the inhibition effect of taurine (Tau) on the myocarditis induced by Coxsackie virus and adriamycin， and myocardial fibrosis followed by myocarditis and its mechanism .METHODS ①The model of viral myocarditis was built by Coxsackie virus B₃ in mice， meanwhile， mice were treated with Tau 1 000，500 and 250 mg·kg-1·d-1 by gastrointestinal administration. The contents of lactate dehydrogenase (LDH)， aspartate amino transferase （AST），reatine kinase isozyme(CK-MB)and the activity of superoxide dismutase(SOD) in blood serum were assayed respectively. The changes of myocardial ultrastructure were observed by electronic microscope. ②The model of myocarditis in rats was built by intraperitoneal injection of adriamycin(ADR) for 2.5 mg·kg-1·week-1. Meanwhile， rats were treated with Tau 400，200 and 100 mg·kg-1·d-1 by gastrointestinal administration. The contents of LDH，AST，CK， malondialdehyde （MDA）and activity of SOD were measured. TGF-β₁ and TNF-α levels were determined by the ELISA.Histopathology changes were detected by HE staining. RESULTS ①Compared with model group， the contents of LDH，AST and CK-MB of blood serum were significantly reduced and the activity of SOD was markedly enhanced in Tau 1 000 and 500 mg·kg-1·d-1groups（P<0.05 or P<0.01）.The RESULTS of electron microscope showed that Tau relieved myocardial damage induced by Coxsackie virus B₃. ②Compared with model group， the contents of LDH， AST， CK， MDA were decreased in Tau groups (400， 200 mg·kg-1·d-1). The activity of SOD was increased and the contents of TGF-β₁，TNF-α were decreased（P<0.05 or P<0.01）.The cardiac myocytes were arranged disorder. Tau relieved the damages of myocardium caused by adriamycin.CONCLUSION Tau can inhibit the damages of myocardium caused by Coxsackie virus B₃ and adriamycin through antioxidation， inhibit myocardial fibrosis followed by myocarditis by inhibition the expressions of TGF-β₁ and TNF-α.