目的：细胞外信号调节激酶(ERK)与细胞生长，分化，增殖等生理病理过程有密切关系。该研究通过比较ERK1/2在病毒性心肌炎心肌细胞中表达变化及ERK特异性阻断剂PD98059干预后细胞活性的改变，探讨ERK信号传导通路在病毒性心肌炎早期病毒攻击心肌细胞过程中的作用。方法：取新生SD大鼠，采用酶消化法分离得到心肌细胞。将培养细胞分为对照组，柯萨奇B3(CVB3)感染组，20 μmol/L和50 μmol/L PD98059干预组，后3组用柯萨奇B 3M 株感染。采用Westen blot分别测定ERK1/2，ERK激活后产物(P-ERK1/2)表达变化，采用MTT法检测细胞活性，采用细胞病变法计算细胞病变。结果：4组ERK1/2表达总量差异无显著性；CVB3感染组P-ERK1/2表达为 135.57 ± 0.7 高于对照组的 119.41 ± 1.97 ，差异有显著性( P < 0.01 )。经20 μmol/L或 50 μmol/L PD98059干预后心肌细胞P-ERK1/2 表达为 113.75±1.03，42.56±2.17 比感染组细胞低，差异有显著性(均P<0.01)；其中50 μmol/L PD98059干预组P-ERK1/2表达较20 μmol/L组低(P<0.01)。PD98059干预组心肌细胞活性0.53±0.13，0.41±0.04 明显高于感染组0.17±0.04，差异有显著性(P<0.01)；不同浓度PD98059干预组间心肌细胞活性差异无显著性(P>0.05)。PD98059干预组细胞出现细胞病变的时间较感染组晚，程度较感染组轻，感染面积较感染组小。结论：病毒在攻击心肌细胞时启动了ERK信号通路；PD98059能干预病毒对心肌细胞的感染。

OBJECTIVE: Extracellular signal-regulated kinase (ERK) is closely related to cellular growth, differentiation and proliferation. This paper aims at (1) detecting ERK1/2 levels in the myocardial cell of viral myocarditis; (2) assessing the effect of ERK specific inhibitor PD98059 on cell viabilities and (3) studying the role of ERK in early viral myocarditis. METHODS: Myocardial cells from neonatal SD rats were incubated in vitro and were randomly assigned into four groups: a Coxsackievirus B3 (CVB3) group, a 20 μmol/L and a 50 μmol/L PD98059 groups and a Control group. CVB3 group was inoculated with CVB3 solutions. The PD98059 groups were initially inoculated with PD98059 for 30 min and then was inoculated with CVB3 solutions. The Control group was treated with DMEM plus 10% FBS. Western Blot was used to detect the ERK 1/2 levels and ERK activation product (P-ERK1/2) levels. Cell viabilities were measured with MTT assay. Cell cytopathic effect (CPE) was used to evaluate myocardial cell lesions. RESULTS: The ERK1/2 levels were not significantly different among the four groups. P-ERK1/2 levels in the CVB3 group were higher than those of the Control group ( 135.57± 0.71 vs 119.41± 1.97; P< 0.01) and also higher than those of the 20 μmol/L and 50 μmol/L PD98059 groups ( 113.75± 1.03 and 42.56± 2.17 respectively; both P< 0.01). P-ERK1/2 levels in the 20 μmol/L PD98059 group were significantly higher those in the 50 μmol/L PD98059 group (P< 0.01). Myocardial cell viabilities of the PD98059 groups ( 0.53± 0.13 and 0.41± 0.04) were higher than the CVB3 group ( 0.17± 0.04) (P< 0.01). There were no differences in myocardial cell viabilities between the two PD98059 groups. Compared with the CVB3 group, myocardial cell lesions in the PD98059 groups occurred later and were less. CONCLUSIONS: CVB3 infection seems to trigger ERK signal transduction pathway. PD98059 may protect myocardial cells from injuries.