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目的:研究加味黄芪建中汤对脾气虚证肺癌小鼠趋化因子受体4(CXCR4)、趋化因子12(CXCL12)、转化生长因子-β(TGF-β)基因表达的影响。方法:采用苦寒泻下、劳倦、节食的方法建立小鼠脾气虚证小鼠模型,小鼠右腋部皮下接种肿瘤细胞建立Lewis肺癌模型。小鼠分为正常组、脾气虚组、肺癌组、脾气虚肺癌组、脾气虚肺癌黄芪组,其中脾气虚肺癌黄芪组用中药加味黄芪建中汤灌胃,其余各组均用0.9%NaCl溶液灌胃;连续灌胃9 d。Real-time PCR方法检测肿瘤组织CXCR4、CXCL12、TGF-β的mRNA表达。结果:与肺癌组比较,CXCL12 mRNA水平明显增高(P<0.05);与脾气虚肺癌组比较,脾气虚肺癌黄芪组CXCL12 mRNA表达水平明显降低(P<0.01)。肺癌组、脾气虚肺癌组和脾气虚肺癌黄芪组的CXCR4、TGF-β的mRNA表达差异无统计学意义(P>0.05);脾气虚肺癌黄芪组和脾气虚肺癌组CXCL12 mRNA与CXCR4 mRNA的表达呈正相关(P<0.05,P<0.01)。结论:加味黄芪建中汤抑制了肿瘤微环境中的趋化因子CXCL12基因的高表达,影响CXCL12/CXCR4通路,可能通过解除肿瘤微环境免疫抑制网络的形成而达到治疗肿瘤的目的。
Objective: To study the effect of Modified Astragalus Jianzhong Decoction on gene expression of CXCR4, CXCL12 and TGF-β in mice with spleen-qi Deficiency Syndrome. Methods: A mouse model of spleen-qi deficiency syndrome was established by bitter cold diarrhea, fatigue and dieting. Lewis lung carcinoma model was established by inoculating tumor cells into the right axilla of mice. The mice were divided into normal group, spleen qi deficiency group, lung cancer group, spleen deficiency lung cancer group and astragalus group of spleen deficiency lung cancer group. Astragalus group was treated with Astragalus Jianzhong Decoction with traditional Chinese medicine, and the other groups were treated with 0.9% NaCl solution Gavage; continuous gavage 9 d. Real-time PCR was used to detect the mRNA expression of CXCR4, CXCL12 and TGF-β in tumor tissue. Results: Compared with lung cancer group, the level of CXCL12 mRNA was significantly increased (P <0.05). Compared with lung cancer group with spleen deficiency, the expression of CXCL12 mRNA in astragalus group decreased significantly (P <0.01). There was no significant difference in the mRNA expressions of CXCR4 and TGF-β between the lung cancer group, the spleen-deficiency lung cancer group and the spleen-qi deficiency lung cancer group (P> 0.05). The expressions of CXCL12 mRNA and CXCR4 mRNA in the astragalus group (P <0.05, P <0.01). Conclusion: Modified Astragalus Jianzhong Decoction inhibits the high expression of chemokine CXCL12 in the tumor microenvironment, and affects the CXCL12 / CXCR4 pathway. It may achieve the goal of tumor treatment by releasing the immunosuppressive network of tumor microenvironment.