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目的:研究苏芪浸膏在抗小鼠Lewis肺癌转移过程中对T淋巴细胞因子的影响,探讨苏芪浸膏在调节肿瘤炎性微环境中的作用。方法:将100只C57BL/6小鼠随机分为空白对照组、荷瘤模型组、环磷酰胺组、苏木组、苏芪浸膏组,除空白对照组外每只小鼠右腋皮下接种0.2mL Lewis肺癌细胞悬液,观察各组小鼠Lewis肺癌肺转移抑制率;流式细胞术测各组小鼠脾CD4+T淋巴细胞中Th17/Treg细胞百分比的动态变化;ELISA法检测各组小鼠脾CD4+T淋巴细胞培养上清中白细胞介素-17(IL-17)、IL-23、干扰素-γ(IFN-γ)、IL-4、IL-2、IL-6动态水平;RT-PCR法检测各组小鼠CD4+T淋巴细胞Foxp3 mRNA及RORγtmRNA的动态表达水平。结果:就肺转移抑制率而言,苏芪浸膏组优于苏木组(P<0.05),而与环磷酰胺组相似;各荷瘤组小鼠脾Th17/Treg随时间迁移呈上升趋势,除环磷酰胺组外,其它荷瘤组与苏芪浸膏组比较,差异均有统计学意义(P<0.05);Th17细胞的增殖刺激因子IL-23及效应因子IL-17,以及Th17细胞的关键转录因子RORγt mRNA表达水平呈现出与Th17细胞相应的动态改变;Treg细胞的增殖刺激因子IL-6,以及Treg细胞的关键转录因子Foxp3 mRNA表达水平呈现出与Treg细胞相应的动态改变。荷瘤模型组IL-4、IL-6较空白对照组有升高趋势,经苏芪浸膏和环磷酰胺治疗后,在第21天时与荷瘤模型组比较,差异有统计学意义(P<0.05);荷瘤模型组IL-2、IFN-γ与空白对照组比较有下降趋势,经苏芪浸膏治疗后,在第21天时与荷瘤模型组比较,差异有统计学意义(P<0.05)。结论:苏芪浸膏抗Lewis肺癌转移的作用机制部分可能是通过调控炎性微环境、抑制肿瘤局部炎性反应、增强机体免疫功能而实现的。
Objective: To study the effect of Su Qi extract on T lymphocyte factor in anti-mouse Lewis lung carcinoma metastasis, and to explore the role of Su Qi extract in regulating tumor microenvironment. Methods: 100 C57BL / 6 mice were randomly divided into blank control group, tumor-bearing model group, cyclophosphamide group, hematoxylin and astragalus extract group. Except for the blank control group, each mouse was inoculated subcutaneously in the right armpit 0.2mL Lewis lung cancer cell suspension was used to observe the inhibitory rate of lung metastasis of Lewis lung cancer in each group. The percentage of Th17 / Treg cells in splenic CD4 + T lymphocytes of mice in each group was measured by flow cytometry. The levels of IL-17, IL-23, IFN-γ, IL-4, IL-2 and IL-6 in the splenic CD4 + T lymphocyte culture supernatant of mice The dynamic expression of Foxp3 mRNA and RORγt mRNA of CD4 + T lymphocytes in each group were detected by RT-PCR. Results: In terms of lung metastasis inhibition rate, Su Qi extract group was superior to the group of Hematoxylin (P <0.05), but similar to cyclophosphamide group; the spleen Th17 / Treg , Except for cyclophosphamide group, the other tumor-bearing group and Su Qi extract group, the difference was statistically significant (P <0.05); Th17 cell proliferation stimulating factor IL-23 and the effector factor IL-17, and Th17 The expression level of RORγt mRNA, a key transcription factor of cells, showed a dynamic change corresponding to that of Th17 cells. The proliferation of Treg cells, IL-6, and Foxp3 mRNA, a key transcription factor of Treg cells, showed dynamic changes corresponding to Treg cells. The tumor-bearing model group IL-4, IL-6 than the control group had a rising trend, after Su Qi extract and cyclophosphamide treatment, on the 21st day compared with the tumor-bearing model group, the difference was statistically significant (P <0.05). Compared with the control group, IL-2 and IFN-γin the tumor-bearing model group showed a decreasing trend. After treated with Su Qi extract, the difference was statistically significant (P <0.05). Conclusion: The mechanism of the effect of Su Qi extract on Lewis lung cancer metastasis may be partly through the regulation of inflammatory microenvironment, inhibition of tumor local inflammatory reaction and enhancement of immune function.