温补散结方对艾氏腹水癌小鼠生存期及腹水中相关免疫细胞因子的影响

Effects of Wenbu Sanjie decoction on survival time and immunity-related cytokine in ascites in EAC mice

目的观察温补散结方对艾氏腹水癌小鼠生存期及腹水中相关免疫细胞因子的影响。方法腹腔注射方法复制艾氏腹水癌小鼠模型40只,随机分为环磷酰胺对照组、温补散结方高剂量组、温补散结方低剂量组、模型对照组。给药9 d后计算各组小鼠生存期及生命延长率。同样方法造模、分组、给药,9 d后抽取腹腔积液,ABC-ELISA法检测腹水中白细胞介素-4(IL-4)、白细胞介素-12(IL-12)、γ干扰素(IFN-γ)含量。结果温补散结方高、低剂量组生存期均较荷瘤组长,差异具有统计学意义(P<0.01);高剂量组生存期较化疗组长,差异有统计学意义(P<0.05);高、低剂量组生存期比较差异无统计学意义(P>0.05)。温补散结方高、低剂量组腹水中IL-12、IFN-γ含量均较模型组及化疗组高,差异有统计学意义(P<0.01);高、低剂量组IL-4含量较模型组低,差异有统计学意义(P<0.05);高、低剂量组之间IL-12、IFN-γ、IL-4含量差异无统计学意义(P>0.05)。结论温补散结方能延长艾氏腹水癌小鼠模型的生存期,使腹水中IL-12、IFN-γ含量升高,IL-4含量降低,Th1/Th2向Th1方向漂移而活化肿瘤浸润淋巴细胞发挥抗瘤作用。

Objective To observe the effect of Wenbu Sanjie（WBSJ） decoction on the survival time and the immunity-related cytokine in ascites in the EAC mice. Methods The 40 ascites mice model, induced by EAC cell suspension intraperitoneal injection, were randomly divided into cyclophosphane control, high dose and low dose WBSJ decoction, and model control groups. The survival time and life-prolonged rate were counted after 9 days. The other mice, modelling, grouping and administration with same way, were sacrificed 9 days after drug administration, and the level of Interleukin-4（IL-4）, Interleukin-12（IL-12）, Interferon-γ（IFN-γ） in ascites were measured by ELISA. Results The survival time in high and low dose WBSJ group were longer than that in both model group （P〈0.05） and cyclophosphane control group（P〈0.05）, but the difference between was high and lower dose groups was not statistically significant （P〉 0.05）. The levels of IL-12, INF-γ in escites were significantly higher than that in model and cyclophosphane groups（P〈0.01）; the levels of IL-4 in high and low dose group were significant ly lower than that in model group （P〈0.01）; the levels of IL-12, IL-4, INF-γin escites were not statistically different between high and low dose group（P〈0.05）. Conclusions WBSJ decoc- tion can prolong the survival time of model mice with EAC cells transplanted, increase the level of IL-12 and INF-γ and decrease the level of IL-4 in the mice.