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目的:观察人工蛹虫草子实体(CCM)对Lewis肺癌移植瘤生长与转移的作用,同时检测CCM对荷瘤鼠CD4+CD25+调节性T细胞的影响,探讨其治疗肿瘤的免疫调节机制。方法:建立Lewis肺癌移植肿瘤模型。给予CCM处理后,观测肿瘤体积动态变化,计数转移灶数目,计算抑瘤率;采用流式细胞术分别于肿瘤生长第6、11、16和21d检测荷瘤鼠脾细胞CD4+CD25+的比例;荧光定量RT-PCR检测肺转移灶组织Foxp3和TGF-βmRNA的表达水平。结果:CCM可抑制Lewis肺癌移植肿瘤的生长与转移,肿瘤生长的早期这种抑制作用比较明显,在肿瘤生长21d抑制率虽为28.6%,但治疗组肺转移灶数目明显降低,P<0.01。与模型组相比,CCM治疗组CD4+CD25+T细胞增高缓慢,在肿瘤生长21d时,模型组脾脏CD4+CD25+T细胞比例为17.0%,而CCM组为13.5%,两者差异有统计学意义,P<0.01。CCM组肺转移灶组织Foxp3和TGF-βmRNA的表达也明显低于模型组。结论:CCM抑制肿瘤生长和转移作用可能与CCM下调荷瘤体内CD4+CD25+T细胞,抑制TGF-β分泌,从而激发机体的抗肿瘤免疫相关。
Objective: To observe the effect of artificial Cordyceps militaris fruiting bodies (CCM) on the growth and metastasis of Lewis lung carcinoma xenografts and to detect the effect of CCM on CD4 + CD25 + regulatory T cells in tumor-bearing mice and to explore its immunoregulatory mechanisms. Methods: Lewis lung carcinoma model was established. After treatment with CCM, the dynamic changes of tumor volume were observed, the number of metastasis was counted and the inhibition rate was calculated. The proportion of CD4 + CD25 + in spleen cells of tumor-bearing mice was detected by flow cytometry on the 6th, 11th, 16th and 21st days respectively. Fluorescent quantitative RT-PCR was used to detect the expression of Foxp3 and TGF-βmRNA in lung metastases. Results: CCM could inhibit the growth and metastasis of Lewis lung carcinoma transplanted tumor. This inhibition was obvious in the early stage of tumor growth. Although the inhibition rate was 28.6% at 21d after tumor growth, the number of lung metastasis in treatment group was significantly decreased (P <0.01). Compared with the model group, the CD4 + CD25 + T cells increased slowly in the CCM-treated group. At 21d, the proportion of splenic CD4 + CD25 + T cells in the model group was 17.0% and that in the CCM group was 13.5% Significance, P <0.01. The expression of Foxp3 and TGF-βmRNA in CCM group was also significantly lower than that in model group. CONCLUSION: CCM can inhibit the growth and metastasis of tumor cells by downregulating CD4 + CD25 + T cells in CCMs and inhibiting the secretion of TGF-β, so as to stimulate the anti-tumor immunity of CCM.