细胞外信号调节激酶信号转导通路在病毒性心肌炎心肌细胞中的调控作用  

Role of extracellular signal-regulated kinase signal transduction pathway in viral myocarditis

作　　者：彭华[1] 刘亚黎[1] 胡晓华[1] 林雯[1] 蒙冰[1] 陈立敏[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院儿科,湖北武汉430022

出　　处：《中国当代儿科杂志》2004年第4期294-296,共3页Chinese Journal of Contemporary Pediatrics

摘　　要：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PD980 5 9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 ,2 0 μmol/L和 5 0 μmol/LPD980 5 9干预组 ,后 3组用柯萨奇B3M株感染。采用Westenblot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 .5 7± 0 .71高于对照组的 119.4 1± 1.97,差异有显著性 (P <0 .0 1)。经 2 0 μmol/L或 5 0 μmol/LPD980 5 9干预后心肌细胞P ERK 1/ 2表达为 113.75± 1.0 3,4 2 .5 6± 2 .17比感染组细胞低 ,差异有显著性 (均P <0 .0 1) ;其中 5 0 μmol/LPD980 5 9干预组P ERK1/ 2表达较 2 0 μmol/L组低 (P <0 .0 1)。PD980 5 9干预组心肌细胞活性 0 .5 3± 0 .13,0 .4 1± 0 .0 4明显高于感染组 0 .17± 0 .0 4 ,差异有显著性 (P <0 .0 1) ;不同浓度PD980 5Objective 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.

关 键 词：细胞外信号调节激酶 信号转导 病毒性心肌炎 

分 类 号：R542.2[医药卫生—心血管疾病]