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目的:观察单宁酸体外抑制痘苗病毒(VACV)感染的效果,探讨单宁酸干扰病毒入侵宿主细胞膜脂的效应机制。方法:基于痘苗病毒细胞感染模型,在病毒吸附前、吸附后和吸附同时3种情况下分别添加单宁酸,采用中性红比色法检测单宁酸对VACV的抑制作用,利用荧光偏振法和流式细胞术分别测定VACV对细胞膜流动性和膜电位的影响及单宁酸的干预作用。结果:单宁酸以病毒吸附后及病毒吸附同时2种方式加入时可抑制VACV感染,半数抑制浓度(IC50)分别为8.7和13.1μg/m L,治疗指数(TI)分别为9.3和6.2;VACV感染可增加细胞膜流动性,单宁酸在病毒吸附后作用,可显著降低细胞膜流动性;VACV感染使细胞膜电位绝对值增大,单宁酸对VACV感染引起的细胞膜超极化状态没有明显影响。结论:单宁酸具有明显的体外抑制VACV感染宿主细胞的作用,其机制可能与拮抗因病毒感染所致的细胞膜流动性升高的膜脂干扰效应有关。
OBJECTIVE: To observe the effect of tannic acid in inhibiting VACV infection in vitro and to explore the mechanism of tannic acid interfering with the invasion of host cell membrane lipids by tannic acid. Methods: Based on the model of cell infection of vaccinia virus, tannic acid was added before, during and after adsorption respectively. Neon red colorimetry was used to detect the inhibitory effect of tannic acid on VACV. Fluorescence polarization And flow cytometry were measured VACV membrane fluidity and membrane potential and tannic acid intervention. Results: The tannic acid could inhibit VACV infection by both virus adsorption and virus adsorption. The IC50 values of tannic acid were 8.7 and 13.1 μg / m L, respectively, and the therapeutic indexes (TI) were 9.3 and 6.2, respectively. VACV infection can increase the membrane fluidity, tannic acid role in the virus adsorption, can significantly reduce cell membrane fluidity; VACV infection increases the absolute value of cell membrane potential, tannic acid on VACV infection caused by membrane hyperpolarization state had no significant effect . CONCLUSION: Tannic acid has a significant inhibitory effect on VACV-infected host cells in vitro. The mechanism may be related to the antagonism of the membrane lipid-lipid interference caused by increased cell membrane fluidity caused by virus infection.