【摘 要】
：
目的 探讨登革病毒诱导EA.hy926细胞(人脐静脉内皮细胞融合细胞株)相对活力的变化与线粒体膜电位(mitochondrial membrane potential,△ψ m)改变及线粒体凋亡途径的关系
【机 构】
：
广东省妇幼保健院医学遗传中心广州511442
【出 处】
：
广东省遗传学会第九届代表大会暨学术研讨会
论文部分内容阅读
目的 探讨登革病毒诱导EA.hy926细胞(人脐静脉内皮细胞融合细胞株)相对活力的变化与线粒体膜电位(mitochondrial membrane potential,△ψ m)改变及线粒体凋亡途径的关系.方法 用登革病毒2型(Dengue Virus Type2,DENV2)感染EA.hy926细胞,MTT法检测感染前后EA.hy926细胞的相对活力,免疫荧光术和流式细胞术分别观察感染前后JC-1在EA.hy926细胞线粒体内的聚集情况以检测△ψm的改变,并通过荧光法检测caspase9的活性变化.结果 DENV2感染EA.hy926后24h、36h及48h后,细胞活性受到显著抑制,550nm处的OD值均低于未感染组,差异有统计学意义(t=-2.39,9.12,5.12；P＜0.01～0.05)；JC-1染色显示,感染后各时间点,代表正常线粒体的红色荧光均较未感染组减弱,而代表△ψm下降的绿色荧光较未感染组逐渐增强.流式检测△ψm平均荧光密度比也较未感染组减低,差异有统计学意义.DENV2感染后早期即可出现caspase9活性的上升,与未感染组相比,各时间点的活性差异均有统计学意义(P＜0.01).结论 DENV2感染EA.hy926细胞后可通过诱发△ψm的下降、激活caspase9的活性,进而启动线粒体的凋亡途径.
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