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作 者:万朝敏[1] 彭文珍[1] 高云钦 王德诚 刘惠莲[1] 王正荣
机构地区:[1]华西医科大学附属第二医院儿科
出 处:《中华儿科杂志》1998年第9期531-533,共3页Chinese Journal of Pediatrics
基 金:国家自然科学基金
摘 要:目的探讨病毒性心肌炎时病毒直接损伤心肌细胞的发病机理。方法培养新生BALB/c小鼠的离体心肌细胞,加柯萨奇B3病毒,造成病毒对心肌细胞直接损伤的细胞模型,检测心肌细胞力学和心肌收缩蛋白分子———心肌肌凝蛋白的α重链(αMHC),β重链(βMHC)的基因表达。结果柯萨奇B3病毒对体外培养的心肌细胞有高度的易感性,并造成收缩力下降,其中感染24小时的心肌细胞收缩力减弱比12小时更为明显;感染后的心肌细胞收缩蛋白分子发生了改变,表现为αMHC含量降低(由0.15±0.02减少到0.13±0.06),而βMHC含量增加(由0.087±0.008增加到0.111±0.009)。结论病毒直接损伤心肌细胞,使心肌细胞收缩蛋白分子的结构发生了改变。Objective To determine the mechanism responsible for direct damage of cardiac muscle cell by virus in myocarditis. Methods Cellular model of directly injuried cardiac muscle cell by Coxsackievirus B3(CVB3) was established by adding CVB3 into the culture of cardiac muscle cells to detect cardiac muscle cell mechanics and the genes expression of myocardial contractile protein, αmyosin heavy chain (αMHC) and βMHC. Results Cultured cardiac muscle cell was susceptible to CVB3. The contractility of cardiac muscle cell infected by CVB3 decreased significantly as compared with normal cardiac muscle cell and decreased more significantly at 24 hours than at 12 hours after infection by CVB3. The gene expression of αMHC mRNA by cardiac muscle cell infected by CVB3 was significantly decreased (from 0.15±0.02 to 0.13±0.06) but that of βMHC mRNA was increased (from 0.087±0.008 to 0.111±0.009) as compared with normal cardiac muscle cells. Conclusion CVB3 may directly damage cardiac muscle cell, alter the structure of myocyte contractile proteins and therefore reduce the cardiac muscle cell contractility.
分 类 号:R725.422.1[医药卫生—儿科]
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