肠道病毒71型感染UT-SCC-60A对细胞周期阻滞和细胞凋亡发生的研究

Cell cycle arrest and apoptosis in enterovirus 71-infected human tonsillar epithelial cells UT-SCC-60A

目的研究肠道病毒71型感染人扁桃体上皮细胞UT-SCC-60A后对细胞周期阻滞和细胞凋亡发生情况。方法以人扁桃体上皮细胞UT-SCC-60A为细胞模型,CCK8试剂盒和流式细胞仪检测Ev71感染UT-SCC-60A后细胞增殖抑制率、凋亡发生和细胞周期阻滞情况。结果EV71对UT-SCC-60A呈现感染时间依赖性抑制,感染48h后抑制率达92.6%;不同剂量的EV71感染均能够显著抑制UT-SCC-60A增殖。EV71感染使UT-SCC-60A以剂量依赖性发生以早期凋亡为主的细胞凋亡,EV71以感染复数为0.5和1感染12h后,早期凋亡细胞比例分别为21.4%和27.1%。EV71感染UT-SCC-60A后使细胞周期阻滞在S期且G0/G1比例下降,EV71以感染复数为1感染12h后,S期比例由对照组的19.0%上升至31.1%,G0/G1期比例由59.8%下降至45.9%。结论Ev71通过使UT-SCC-60A发生S期阻滞来抑制细胞增殖且诱导以早期凋亡为主的细胞凋亡。

Objective To investigate cell cycle arrest and apoptosis of human tonsillar epithelial cell UT-SCC-60A induced by enterovirus71(EV71).Methods Human tonsillar epithelial cell UT-SCC-60A was chose as a cell model,inhibition rate,apoptosis and cell cycle arrest of EV71-infected UT-SCC-60A were determined by CCK8kit and flow cytometry.Results EV71 inhibited proliferation of UT-SCC-60A in a time-dependent manner,the inhibition rate achieved 92.6% after EV71 infected 48 h.Different multiplicities of infection (MOI)of EV71 at 0.5and 1could significantly inhibited UT-SCC-60A.EV71 induced UT-SCC-60A occurred apoptosis,especially early apoptosis in a dosage-dependent manner,the rates of early apoptosis of UTSCC-60A reached 21.4% and 27.1% when EV71 infected with MOI at 0.5and 1at 12h post of infection.The cell cycle arrested at S phase in EV71 infected UT-SCC-60A and the percentage of G0/G1 phase was declined,the percentage of S phase was ascended from 19.0%to 31.1% compared with mock group.However,the percentage of G0/G1 phase was declined from 59.8%to 45.9%when UT-SCC-60A was infected with EV71 with MOI at 1at 12h post of infection.Conclusions EV71 inhibits proliferation of UT-SCC-60A through inducing S phase arrest and induces early apoptosis.