摘要
目的研究番荔枝单体Bullatacin对C57BL/6J小鼠接种H22肝癌细胞形成移植瘤的作用及其影响。方法将雌雄各半C57BL/6J小鼠分为空白对照组、模型组、Bullatacin干预组和顺铂对照组,每组10只,每只接种H22细胞数量1×106。Bullatacin浓度100μg·m L^(-1),每次0.1 m L腹腔注射,每天1次,连续3天,14天后取材。结果 Bullatacin可抑制移植瘤的生长,其疗效优于顺铂组(P<0.05)。免疫组化结果显示Bullatacin可抑制移植瘤Ki67的表达。C57BL/6J小鼠空白对照组淋巴细胞表达白介素-4(IL-4)的阳性率为(17.3±0.35)%,而在形成移植瘤后为(24.2±0.32)%,Bullatacin干预后为(12.7±0.35)%,顺铂对照组为(11.2±0.33)%。C57BL/6J小鼠空白对照组淋巴细胞γ-干扰素(IFN-γ)的阳性率为(13.4±0.34)%,而在形成移植瘤后为(5.6±0.33)%,顺铂对照组为(6.2±0.35)%,Bullatacin干预后为(14.3±0.33)%。通过淋巴细胞分析表明,移植瘤使Th1/Th2漂移,而Bullatacin可使Th1/Th2向正常转化,顺铂则无此作用。C57BL/6J小鼠的血清IFN-γ含量为(132.2±6.7)pg·m L^(-1),接种H22后为(98.9±6.8)pg·m L^(-1),使用顺铂后为(77.5±7.0)pg·m L^(-1),而在Bullatacin干预后达到(161.5±6.5)pg·m L^(-1)。C57BL/6J小鼠的血清IL-4为(6.20±1.0)pg·m L^(-1),接种H22形成移植瘤后显著升高,达到(16.25±1.1)pg·m L^(-1),顺铂干预后为(3.70±1.1)pg·m L^(-1),使用Bullatacin干预后为(6.51±1.2)pg·m L^(-1),空白组、模型组和Bullatacin干预之间的差异具有统计学意义(P<0.05)。结论番荔枝单体Bullatacin可以有效缩小H22肝癌细胞形成的移植瘤,促进Th1/Th2恢复至平衡状态。
Objective To study the effect and immune mechanism of Bullatacin on tansplanted tumor of C57BL/6J mice inoculated with H22 liver cancer cells. Methods The C57BL/6J mice were divided into blank control group, model group, Bullatacin intervention group, and Cisplatin control group. Every mouse was inoculated with 1 × 10^6 H22 cells. The concentration of Bullatacin was 100μg·mL^-1. Bullatacin was administered by intraperitoneal injection with a dose of 0.1mL, once daily, for 3 consecutive days. The samples were taken after 14 days. Results Bullatacin could significantly inhibit the growth of transplanted tumor. The therapeutic effect of Bullataein group was better than that of cisplatin control group （P〈0.05）. The immunohistochemical results showed that Bullatacin could inhibit the positive rate of transplanted tumor Ki67. The positive rate of lymphocyte IL-4 of C57BL/6J mice in blank control group was （17.3 ± 0.35） %. It changed to be （24.2 ± 0.32） % when transplanted tumor formed and （12.7 ± 0.35） % after intervened by Bullatacin, and it was （11.2 ± 0.33） % in the Cisplatin control group. In blank control group, the positive rate of lymphocyte IFN-γ was （13.4 ± 0.34） %, and it turned to be （5.6 ± 0.33） % after transplanted tumor formed and （14.3 ± 0.33） % after intervened by Bullatacin, but it was （6.2 ±0.35） % after treated by Cisplatin. The analysis of spleen lymphocyte showed that the transplanted tumor caused Th1/Th2 to drift, but Bullatacin could make Th1/Th2 transform back to normal, while Cisplatin showed no such effect. The normal content of IFN-γ in blood serum was （132.2 ± 6.7） pg·mL^-1. It was decreased to （98.9 ± 6.8） pg·mL^-1 after inoculation of H22 and to （77.5 ± 7.0） pg·mL^-1 after intervention of Cisplatin, but raised to （161.5 ± 6.5） pg·mL^-1 after Bullatacin intervention. The IL-4 level was （6.20 ± 1.0）pg·mL^-1 in normal blood serum. It increased significantly up to （16.25 ± 1.1） pg·mL^-1 after inoculation of H22, but decreased to （6.51 ± 1.2） pg·mL^-1 after Bullatacin intervention and to （3.70 ± 1.1） pg·mL^-1 after Cisplatin intervention. There were statistically significant differences between blank control group, model group and Bullatacin intervention group （P 〈 0.05）. Conclusion Sirikaya lactone BuUatacin has anti-tumor effect, as it could reduce tumor and help regulate the Th1/Th2 balance in mice.
出处
《肿瘤药学》
CAS
2016年第4期266-270,280,共6页
Anti-Tumor Pharmacy
基金
广州市番禺区科技计划项目(2009-Z-110-1)
广东省建设中医药强省项目(20151045)
广东省医学科研基金(B2016098)
