中文摘要：

目的探讨桂皮醛（CA）对柯萨奇病毒B3（CVB3）诱发的小鼠病毒性心肌炎（VMC）作用及其机制。方法除正常对照组外,其他小鼠经腹腔注射CVB3m0.1mL建立病毒性心肌炎BALB/c小鼠模型。于接种病毒72h后,CA不同剂量治疗组分别灌胃给予CA22.5,28.1,37.5mg·kg^-1,RA组腹腔注射黄芪注射液50mg·kg^-1,模型组与正常对照组灌胃给予0.9%氯化钠溶液2500mg·kg^-1,连续给药21d。观察接种病毒后第7天心肌组织病理学变化,测定血清乳酸脱氢酶（LDH）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）含量;测定接种病毒后第14天血清一氧化氮（NO）含量,第14天心肌诱导型一氧化氮合酶（iNOS）以及核因子κB（NF-κB）表达,行心肌组织光镜病理检查与评分;第21天行心肌组织光镜病理检查。计算小鼠累积死亡率和中位生存时间。结果与模型组比较,CA28.1,37.5mg·kg^-1治疗组小鼠死亡率显著降低（均P〈0.01）,中位生存时间延长,感染第7天心肌病毒滴度降低,血清CK、CK-MB、LDH释放减少（均P〈0.05）。血清NO含量明显降低（P〈0.01）,感染第14天心肌iNOS、NF-κB表达（P〈0.05）与病理评分均明显改善。结论CA有治疗CVB3m诱发的小鼠病毒性心肌炎作用,其作用机制可能与抑制NF-κB与iNOS表达相关。

英文摘要：

Objective To investigate the therapeutic effect of cinnamaldehyde （CA） on mice viral myocarditis caused by coxsackievirus B3 （CVB3 ）. Methods One hundred and seventy male Balb/c mice were randomly divided into 6 groups. The mice in the control group （ n = 20 ） was i. p injected with normal saline, those in other five groups （ n = 30 in each ） were inoculated with Coxsackievirus B3 m virus and bred in insulation lab. After viral inoculated for 72 h, Groups CA were i. g injected with CA at dose of 22.5,28.1,37.5 mg ·kg^-1 , respectively. Model group was treated with normal saline ; Group RA was i. p. treated with 50 mg ·kg^-1 Radix astragali injective solution（RA） as a positive control. All groups were treated for 10 d. The heart histopathologic changes, content of CK, CK-MB, LDH and NO in serum, and iNOS, NF-κB in myocardium were detected. Results The histopathologic score, death rate, median survival time,and the content of CK, CK-MB,LDH in serum were lower in 22.5,28.1,37.5 mg ·kg^-1 CA groups than those in the model group at 7 d after viral inoculation（ P 〈 0.05）. The content of NO in serum,expression of NF-κB and iNOS in myocardium were lower in 22.5,28.1,37.5 mg ·kg^-1 CA groups than those in model group at 14 d after viral inoculation （ P 〈 0. 05 ）. The histopathologic changes （ necrosis, degeneration and cellular infiltration） were lighter in CA groups than those in model group at 21 d after viral, inoculation. Conclusion CA has a significant therapeutic effect on experimental VMC, the mechanism of which may be associated with inhibition of NF-κB and iNOS expressions.