CAJ | 학술논문

目的探讨病毒直接损伤心肌细胞的机制.方法采用柯萨奇B3病毒感染体外培养心肌细胞,检测心肌细胞收缩力以及心肌细胞的α-MHC和β-MHC的基因表达,并与正常心肌细胞相对比.结果柯萨奇B3病毒感染后的心肌细胞收缩力比正常心肌细胞的心肌收缩力明显降低(P<0.01), 并且感染后24 h比12 h下降更为显著(P<0.05);心肌细胞收缩蛋白α-MHC和β-MHC的基因表达也发生了改变, 柯萨奇B3病毒感染后心肌细胞的α-MHC基因表达明显降低,而β-MHC基因表达升高.结论柯萨奇B3病毒感染后的心肌细胞收缩力下降,使心肌细胞以α-MHC基因表达为主转向以β-MHC基因表达为主.
목적탐토병독직접손상심기세포적궤제.방법채용가살기B3병독감염체외배양심기세포,검측심기세포수축력이급심기세포적α-MHC화β-MHC적기인표체,병여정상심기세포상대비.결과가살기B3병독감염후적심기세포수축력비정상심기세포적심기수축력명현강저(P<0.01), 병차감염후24 h비12 h하강경위현저(P<0.05);심기세포수축단백α-MHC화β-MHC적기인표체야발생료개변, 가살기B3병독감염후심기세포적α-MHC기인표체명현강저,이β-MHC기인표체승고.결론가살기B3병독감염후적심기세포수축력하강,사심기세포이α-MHC기인표체위주전향이β-MHC기인표체위주.
Objective To determine the mechanisms of direct virus injury to cardiac myocytes. Method Cardiac myocyte mechanics and gene expression of the myocardial contractile proteins α-myosin heavy chain(α-MHC) and β-myosin heavy chain (β-MHC)in normal cardiac myocytes Coxsackievirus B3 were analysed. Result Contractility was significantly lower in infected cardiac myocytes than in normal cardiac myocytes(P<0.01). The decrease in contractility was more significant at 24 h than at 12 h after infection(P<0.05). The level of mRNA for myocardial contractile protein α-MHC was significantly lower in cardiac myocytes(0.1274) infected with Coxsackievirus B3 than in normal myocytes(0.1529).However, the mRNA level for β-MHC was significantly higher in infected myocytes(0.1108) than in normal myocytes(0.0872). Conclusion Myocyte contractility may be reduced because the infection with Coxsackievirus B3 may affect gene expression of myocyte contractile proteins; viral injury may cause a shift of protein expression from preponderance of α-MHC to prepouderance of β-MHC.