摘要
目的研究负载抗原的树突状细胞(DC)联合细胞因子诱导的杀伤细胞(CIK)对肝癌细胞株HepG2/ADM多药耐药性的逆转作用。方法 HepG2/ADM细胞冻融抗原冲击DC,联合CIK细胞与HepG2/ADM细胞共培养,以未负载抗原的DCCIK作为阴性对照,以未经共培养处理的HepG2/ADM细胞作为空白对照。采用流式细胞仪在细胞处理后不同时间点检测HepG2/ADM细胞内罗丹明-123(R-123)浓度和阿霉素(ADM)浓度,采用Western blot检测细胞内P-糖蛋白(P-gp)水平。结果与DC-CIK共培养相比,负载抗原的DC-CIK共培养能够明显抑制HepG2/ADM细胞内R-123的外排,提高细胞内ADM浓度,同时降低细胞内P-gp水平(P<0.05)。结论经抗原冲击的DC和CIK共培养可明显抑制HepG2/ADM细胞内R-123的外排,提高细胞内ADM浓度,抑制P-gp表达,从而有效逆转肝癌细胞多药耐药性。
Objective To analyze the reversal effects of antigen‐loaded dendritic cells （DC ） and cytokine‐induced killer cells （CIK） on multidrug resistance of hepatocarcinoma line HepG2/ADM cells .Methods DC were impacted with HepG2/ADM cell ly‐sages and were co‐cultured with CIK .Intracellular concentration of rhodamine‐123（R‐123） and adriamycin（ADM ） were determined by flow cytometry ,and the expression of P‐glycoprotein（P‐gp） was detected by Western blot .Results Compared with non‐antigen‐loaded DC‐CIK ,antigen‐loaded DC‐CIK remarkably increased the intracellular concentration of R‐123 ,and increased the concentra‐tion of ADM ,as well as decreased the expression of P‐gp（P〈0 .05） .Conclusion Antigen‐loaded DC‐CIK could increase the concen‐tration of intracellular ADM ,and decrease the expression of P‐gp ,thus could reverse multidrug resistance of hepatocarcinoma cells .
出处
《检验医学与临床》
CAS
2016年第13期1758-1759,共2页
Laboratory Medicine and Clinic
基金
重庆市渝中区科技计划项目(20120225)
