目的 探讨喜树碱体外抗单纯疱疹病毒I型（HSV-1）的作用及其机制。方法 不同浓度的喜树碱作用于HSV-1感染的Vero细胞后，采用细胞病变（cytopathologic effects，CPE）法评价喜树碱体外抗HSV-1的作用，计算喜树碱半数毒性浓度（TC₅₀）、病毒半数抑制浓度（IC₅₀）及治疗指数（TI），并通过实时荧光定量PCR（RT-qPCR）法检测喜树碱对HSV-1相关基因mRNA表达的影响。结果 喜树碱的TC₅₀为2 153.44 nmol/L，IC₅₀为43.01 nmol/L，TI为50.07。RT-qPCR结果显示，喜树碱能明显抑制HSV-1 UL12、UL42、UL54、TK基因的表达，其抑制作用与喜树碱浓度呈剂量依赖关系。结论 喜树碱具有明显抗HSV-1的作用，能抑制HSV-1 UL12、UL42、UL54、TK基因的转录。

Objective To study the antiviral effect and mechanism of camptothecin against HSV-1 in vitro. Methods Adding different concentration of camptothecin to the Vero cells infected by HSV-1, the measure of cytopathologic effects (CPE) was taken to evaluate the result of antiviral effect and mechanism of camptothecin. The median toxic concentration (TC₅₀), median inhibitory concentration (IC₅₀), and therapeutic index (TI) of camptothecin were calculated, and the affection of camptothecin on HSV-1 mRNA expression was examined through the method of RT-qPCR. Results TC₅₀ of camptothecin was 2 153.44 nmol/L, IC₅₀ was 43.01 nmol/L, and TI was 50.07. The results of RT-qPCR showed that camptothecin can significantly inhibit the gene transcription of HSV-1, UL12, UL42, UL54, and TK, and its inhibitory effect was in dose-dependence relationship with the concentration of camptothecin. Conclusion Camptothecin has an obvious antiviral effect on HSV-1 and can inhibit the transcription of HSV-1 genes such as UL12, UL42, UL54, and TK.

国家自然科学基金面上项目（81173637）；国家级“大学生创新创业项目训练计划”项目（201713705038）