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目的观察启膈散对食管癌细胞干预树突状细胞成熟的影响。方法制备条件培养基,用Fieoll密度梯度离心法分离外周血单个核细胞,体外诱导培养树突状细胞(Dendritic Cells,DCs),流式细胞术检测DCs表面标志物,MTT法检测淋巴细胞细胞增殖;LDH释放法检测细胞毒T淋巴细胞(cytotoxic T lymphocyte,CTL)杀伤力;ELISA检测细胞因子分泌,Western blot检测STAT3蛋白表达。结果食管癌EC9706细胞条件培养基可以减少外周血单核细胞诱导的树突状细胞表达CD80、CD86、CD1a,抑制DCs刺激淋巴细胞增殖和减弱CTL的杀伤力,减少IL~(-1)2分泌,增加STAT3蛋白表达和磷酸化;与肿瘤条件培养基相比,启膈散条件培养基组DCs CD80、CD86、CD1a增加,淋巴细胞的增殖能力、CTL杀伤作用增强,IL~(-1)2分泌增加,STAT3蛋白表达和磷酸化减少。结论启膈散可以通过STAT3信号通路减弱食管癌细胞上清对树突状细胞成熟的影响。
Objective To observe the effects of Qige San on the intervention of esophageal cancer cells in dendritic cells. Methods Conditioned medium was prepared. Peripheral blood mononuclear cells were isolated by Fieoll density gradient centrifugation. Dendritic cells (DCs) were cultured in vitro. The surface markers of DCs were detected by flow cytometry. The proliferation of lymphocytes was detected by MTT assay. ; LDH release assay cytotoxic T lymphocyte (CTL) lethality; cytokines secretion by ELISA, STAT3 protein expression by Western blot. Results EC9706 cells conditioned medium could reduce the expression of CD80, CD86 and CD1a on dendritic cells induced by peripheral blood mononuclear cells, inhibit the proliferation of lymphocytes stimulated by DCs, attenuate the cytotoxicity of CTL and decrease the secretion of IL - 1 2 , And increased STAT3 protein expression and phosphorylation. Compared with tumor-conditioned media, CD80, CD86 and CD1a of DCs increased, lymphocyte proliferation and cytotoxicity of CTLs increased, IL-1 2 Increased secretion, STAT3 protein expression and phosphorylation decreased. Conclusion Qige San can attenuate the effect of esophageal cancer cell supernatant on dendritic cell maturation through STAT3 signaling pathway.