Song Xiao-Dong, Liu Zhe, Chen Jing-Zhou, Sun Kai, Hui Ru-Tai
Key Laboratory of Clinical Cardiovascular Genetics, Ministry of Education (Sino-German Laboratory for Molecular Medicine), Fu Wai Hospital, CAMS and PUMC, Beijing 100037, China.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2010 Jun;32(3):293-6. doi: 10.3881/j.issn.1000-503X.2010.03.012.
To investigate the effects of Qihong capsule (QH) on HeLa cells infected by coxsackievirus B3 (CVB3) in vitro and its potential antiviral mechanism.
HeLa cells were infected by CVB3 in vitro. XTT assay and plaque inhibition assay were performed to determine the 50 % effective dose, (ED50), 50 % inhibitory concentration (IC50), and 50% cytotoxicity concentration (CC50) of QH and the control drug, ribavirin. The total therapeutic index (TI) was calculated. Anti-viral time-course experiments were performed to compare the anti-viral effects at different time points. The inhibitory effects of QH on the attachment and penetration of CVB3 were also observed.
XTT assay and plaque inhibition assay showed that the ED50 and IC50 were (7.16+/-0.80) mg/L and (2.63+/-0.50) mg/L in QH group and (4.35+/-0.40) mg/L and (1.92+/-0.30) mg/L in ribavirin group, respectively. CC50 was 16-fold higher in QH group than in ribavirin group QH: (1 648+/-219) mg/L vs. Ribavirin: (103+/-14) mg/L. Time-course studies demonstrated that antiviral effect of QH was mainly found 0-4 hours after infection. QH effectively blocked the attachment and penetration of CVB3 into cells.
By inhibiting the attachment and penetration of CVB3, QH can effectively inhibit the invasion of virus in vitro with low toxicity.
研究芪红胶囊(QH)对体外柯萨奇病毒B3(CVB3)感染的HeLa细胞的影响及其潜在的抗病毒机制。
体外培养HeLa细胞,用CVB3感染。采用XTT法和空斑抑制试验测定QH和对照药物利巴韦林的50%有效剂量(ED50)、50%抑制浓度(IC50)和50%细胞毒性浓度(CC50),计算总治疗指数(TI)。进行抗病毒时间进程实验,比较不同时间点的抗病毒效果。观察QH对CVB3吸附和穿入的抑制作用。
XTT法和空斑抑制试验显示,QH组的ED50和IC50分别为(7.16±0.80)mg/L和(2.63±0.50)mg/L,利巴韦林组分别为(4.35±0.40)mg/L和(1.92±0.30)mg/L。QH组的CC50比利巴韦林组高16倍:QH组为(1648±219)mg/L,利巴韦林组为(103±14)mg/L。时间进程研究表明,QH的抗病毒作用主要在感染后0 - 4小时出现。QH能有效阻断CVB3对细胞的吸附和穿入。
QH通过抑制CVB3的吸附和穿入,能有效抑制病毒在体外的侵袭,且毒性较低。