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酸性微环境对单核/巨噬细胞分泌血管内皮细胞生长因子及Tca8113细胞杀伤作用的影响 被引量:4

Experimental study on the anti-tumor effect of monocytes/macrophages against Tca8113 cells and the secretion of vascular endothelial growth factor in acid microenvironment
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摘要 目的通过酸性微环境下单核/巨噬细胞分泌血管内皮细胞生长因子(VEGF)及对舌癌细胞株Tca8113杀伤作用的研究,探讨肿瘤内浸润的单核/巨噬细胞在酸性微环境影响下的功能状态。方法从健康人的外周血中分离单核细胞并通过培养将其转化为单核/巨噬细胞,分别调整培养液的pH值为酸性:6.6、6.8;常规环境:pH值为7.2,将单核/巨噬细胞和舌癌细胞株Tca8113进行混合培养,MTT法检测单核/巨噬细胞对舌癌细胞的杀伤作用;采用ELISA法检测不同微环境下单核/巨噬细胞VEGF的分泌情况。结果在酸性微环境下,单核/巨噬细胞对舌癌细胞株的杀伤作用低于常规环境下(P<0.05);而分泌VEGF的能力较常规环境下增强(P<0.05)。结论可能正是肿瘤组织局部的酸性微环境改变了单核/巨噬细胞的功能,更多的参与了肿瘤的生长,但其在肿瘤中的具体机制及如何调节单核/巨噬细胞在肿瘤组织中的功能还需进一步的研究。 Objective To investigate the anti-tumor effect of monocytes/macrophages against Tca8113 cells and the secretion of vascular endothelial growth factor(VEGF) in acid microenvironment in vitro.Methods Peripheral blood mononuclear cells were extracted from healthy person' s blood and cultivated to transform into monocytes/macrophages.The monocytes/macrophages were cultured with Tca8113 in acid microenvironment(pH6.6 and pH6.8) and in normal microenvironmen(tpH7.2).The anti-tumor effect of monocytes/macrophages against Tca8113 cells were examined by MTT assay.The expression of VEGF was detected by enzyme-link immunoassay(ELISA).Results The anti-tumor effect of monocytes/macrophages against Tca8113 cells in acid environment was lower than in normal environment(P〈0.05).VEGF excreted by mononuclear/macrophage was significantly higher in acid microenvironment than in normal microenvironment.Conclusion Due to acid microenvironment inside tumor,the anti-tumor effect of monocytes/macrophages against tumor cell was decreased,but the secretion of VEGF was gradually increased.However,the function of monocytes/macrophages on anti-tumor need more research.
出处 《华西口腔医学杂志》 CAS CSCD 北大核心 2010年第4期364-366,共3页 West China Journal of Stomatology
基金 国家自然科学基金资助项目(30660200) 贵州省优秀科技教育人才省长专项基金资助项目[(2005)160号]
关键词 单核/巨噬细胞 舌鳞状细胞癌 酸性 血管内皮细胞生长因子 monocytes/mcrophages tongue squamous cell carcinoma acid vascular endothelial growth factor
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共引文献6

同被引文献34

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