The study on intramyocardial calcium overload and apoptosis induced by coxsackievirus B3.

X Hu, H Wang, W Lu, Y Dong, P Cheng
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Abstract

The isolated cardiac myocytes of rats were immediately infected by cosackievirus B3 (CVB3) to investigate the effects of such procedure on the cell cycle, apoptosis and intracellular ionized calcium (Ca2+ i) of cardiac myocytes. Newborn Balb/c murine cardiac myocytes were cultivated, then infected by CVB3. Intracellular Ca2+ i was measured by flow cytometer. The calcium in the medium for culturing cardiac myocytes was detected by using atom absorb spectrum test. It was found that CVB3 could markedly inhibit the differentiation and proliferation of the infected cardiac myocytes and induce the apoptosis. The intracellular Ca2+ i level in the infected group was significantly higher than in the control group (P < 0.01). The calcium concentration in the medium for culturing cardiac myocytes in the infected group was significantly lower than in the control group (P < 0.05). It was suggested that the apoptosis and intracellular calcium overload of the CVB3-affected cardiac myocytes are likely to play an important role in the pathogenesis of viral myocarditis.

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对柯萨奇病毒 B3 诱导的心肌内钙超载和细胞凋亡的研究
将分离的大鼠心肌细胞立即感染柯萨奇病毒 B3(CVB3),以研究该过程对心肌细胞的细胞周期、细胞凋亡和细胞内电离钙(Ca2+ i)的影响。新生 Balb/c 鼠心肌细胞经培养后感染 CVB3。用流式细胞仪测量细胞内 Ca2+ i。用原子吸收光谱测试法检测培养心肌细胞的培养基中的钙。结果发现,CVB3 能明显抑制受感染心肌细胞的分化和增殖,并诱导其凋亡。感染组细胞内 Ca2+ i 水平明显高于对照组(P < 0.01)。感染组心肌细胞培养基中的钙浓度明显低于对照组(P < 0.05)。这表明,受CVB3影响的心肌细胞凋亡和细胞内钙超载可能在病毒性心肌炎的发病机制中起重要作用。
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