雷公藤内酯醇对小鼠H22腹水瘤细胞凋亡及PD|L1表达的影响

目的 探讨雷公藤内酯醇诱导H22腹水瘤细胞凋亡以及作用机制。 方法 采用腹腔注射肝癌H22细胞建立小鼠腹水瘤模型,80只成模小鼠随机分为对照组、雷公藤内酯醇低、中、高剂量(0.05, 0.1, 0.2 mg/kg)组,每组20只。观察小鼠体质量变化、生存期; 计量腹水体积及计数腹水内肿瘤细胞数; 流式细胞仪检测肿瘤细胞凋亡及程序性死亡受体-配体1(PD-L1)表达的变化。 结果 与对照组比较,雷公藤内酯醇3个剂量组小鼠的体质量增长缓慢,生存期中位数均有显著延长(P<0.01); 雷公藤内酯醇低、中、高3个剂量组的腹水体积以及每毫升中的肿瘤细胞数均显著低于对照组(P<0.05); 流式细胞术检测结果显示,不同剂量的雷公藤内酯醇可以显著诱导H22细胞凋亡并下调H22细胞PD-L1的表达(P<0.05,P<0.01)。 结论 雷公藤内酯醇可能通过诱导肝癌H22细胞凋亡及抑制PD-L1表达,发挥抗肝肿瘤的作用。

Effects of Triptolide on Apoptosis and PD-L1 Expressionin H22 Hepatic Ascitic Tumor Cells in Mice

Objective To investigate the effects of Triptolide on apoptosis and PD-L1 expression in H22 hepatic ascitic tumor cells in mice. Method Eighty mice were injected intraperitoneally with H22 cells and divided into 4 groups: control group, low-dose TPL group( 0.05 mg/kg), medium-dose TPL group( 0.1 mg/kg)and high-dose TPL group(0.2 mg/kg). The weight change and survival period of mice were observed; the volume of ascites and the number of tumor cells were counted, and the apoptosis and PD-L1 expression on H22 cells were detected by flow cytometry. Result The TPL groups showed slower body weight increase and longer median survival time than the control group. The volume of ascites and the number of tumor cells decreased compared with the control group. In addition, TPL significantly induced H22 cell apoptosis and down-regulated PD-L1 expression in a dose-manner. Conclusion TPL may play an anti-hepatocellular carcinoma action by inducing H22 cell apoptosis and inhibiting the expression of programmed death receptor ligand 1.