柯萨奇B3病毒对HL-1心肌细胞的影响

Effect of Coxsackievirus B3 on HL-1 myocardium cells

目的探讨柯萨奇B3病毒对HL-1心肌细胞影响。方法实时荧光聚合酶链反应检测柯萨奇B3病毒感染的HL-1心肌细胞Bcl-2及Bax的表达;Annexin V-PE凋亡检测试剂盒检测感染的HL-1心肌细胞发生凋亡的比率,并与未感染心肌细胞进行对比。结果感染后4 h组(0.199±0.005 vs.0.104±0.014,P=0.0008)及24 h组(0.154±0.005 vs.0.104±0.014,P=0.0176)的Bcl-2/Bax表达均显著高于未感染组,差异有统计学意义。感染后4 h组的Bcl-2/Bax表达高于感染后24 h组,差异有统计学意义(0.199±0.005 vs.0.154±0.005,P=0.0009)。感染后4 h组(9.160%±0.161%vs.0.908%±0.015%,P<0.0001)、12 h组(6.305%±0.231%vs.0.908%±0.015%,P<0.0001)、24 h组(3.260%±0.162%vs.0.908%±0.015%,P<0.0001)的心肌细胞凋亡率显著高于未感染组,差异均有统计学意义。感染后4 h组的心肌细胞凋亡率高于感染后12 h组(9.160%±0.161%vs.6.305%±0.231%,P<0.0001)和24 h组(9.160%±0.161%vs.3.260%±0.162%,P<0.0001),差异均有统计学意义。结论柯萨奇B3病毒导致HL-1心肌细胞的凋亡,在感染4 h后增加尤为明显。

Objectives To investigate the effect of Coxsackievirus B3 on HL-1 myoeardium ceils. Methods We examined the expression of Bel-2 and Bax of infection HL-1 myoeardium cells by reai time polymerase chain reaction （PCR）, the apoptosis ratio by Annexin V-PE kit and compared them with those of non-infected HL-1 myocardium cells. Resuits Compared with non-infected group, Bcl-2/Bax of 4 h after infection group （0.199 ± 0.005 vs. 0.104 ± 0.014,P=0.0008） and 24 h after infection group （0.154 ± 0.005 vs. 0.104 ± 0.014,P=0.0176） increased significantiy. Compared with 24 h after infection group, Bcl-2/Bax of 4 h after infection group increased significantly （0.199 ± 0.005 vs. 0. 154 ± 0.005, P=0.0009）. Compared with non-infected group, apoptosis ration of 4 h after infection group （9.160% ±0.161% vs. 0.908% ±- 0.015%, P〈0.0001）, 12 h after infection group （6.305% ± 0.231% vs. 0.908% ± 0.015%, P〈0.0001） and 24 h after infection group （3.260% ±0.162% vs. 0.908% ± 0.015%, P〈0.0001） increased significantly. Compared with 12 h after infection group （9.160% ± 0.161% vs. 6.305% ±0.231%, P〈0.0001 ） and 24 h after infection group （9.160%±0.161% vs. 3.260%±0.162% ,P〈0.0001）, apoptosis ration of 4 h after infection group increased significantly. Conclusions Coxsackievirus B3 contributes to the apoptosis of HL-1 cells, especially 4 h after infection. Key words ： myocarditis ; myocardium cells ; Coxsackievirus B3 ; apoptosis