Matsumori A, Tomioka N, Kawai C
Department of Internal Medicine, Kyoto University, Japan.
Am Heart J. 1988 Jun;115(6):1229-32. doi: 10.1016/0002-8703(88)90013-0.
The effects of recombinant human leukocyte interferon alpha-A/D on experimental myocarditis caused by coxsackievirus B3 were investigated. Four-week-old male C3H/He mice were inoculated intraperitoneally with 10(5.5) 50% tissue culture infective dose (TCD50) in 0.1 ml of coxsackievirus B3 (Nancy strain). Interferon alpha-A/D, 10(4) U/gm/day, was administered subcutaneously daily, starting 1 day before (group 1) or on the day of (group 2) infection. Animals were killed on day 7. The infectivity of myocardial virus was significantly lower in group 1 (0.7 +/- 0.1 log10TCD50/mg, p less than 0.005) and in group 2 (2.5 +/- 1.2 log10TCD50/mg, p less than 0.005) than in control mice (4.4 +/- 0.9 log10TCD50/mg). Results of histologic examination showed extensive myocardial necrosis and cellular infiltration in all mice in the untreated group, but significantly less severe necrosis and infiltration in the treated groups. Thus, interferon alpha-A/D, when given before and simultaneously with virus, effectively inhibited replication of myocardial virus and reduced the inflammatory response and myocardial damage in an experimental model of viral myocarditis.
研究了重组人白细胞干扰素α - A/D对柯萨奇病毒B3所致实验性心肌炎的影响。4周龄雄性C3H/He小鼠腹腔接种0.1 ml含10(5.5) 50%组织培养感染剂量（TCD50）的柯萨奇病毒B3（南希株）。从感染前1天（第1组）或感染当天（第2组）开始，每天皮下注射10(4) U/g体重的干扰素α - A/D。在第7天处死动物。第1组（0.7±0.1 log10TCD50/mg，p＜0.005）和第2组（2.5±1.2 log10TCD50/mg，p＜0.005）心肌病毒的感染性显著低于对照小鼠（4.4±0.9 log10TCD50/mg）。组织学检查结果显示，未治疗组所有小鼠均有广泛的心肌坏死和细胞浸润，但治疗组的坏死和浸润明显较轻。因此，在病毒感染前及同时给予干扰素α - A/D，可有效抑制病毒性心肌炎实验模型中心肌病毒的复制，并减轻炎症反应和心肌损伤。
