冬凌草甲素联合DC-CIK细胞杀伤RPMI 8226细胞的研究  

Effect of DC-CIK cells combined with oridonin on cytotoxicity against RPMI 8226 cells

作　　者：曲佳[1] 詹昱[1] 冯可欣[1] 陈玲珍[1] 巫进明[1] 杨郁青[1] 

机构地区：[1]广州市第十二人民医院血液科,510620

出　　处：《实用医学杂志》2014年第14期2208-2210,共3页The Journal of Practical Medicine

基　　金：广州市卫生局项目(编号:20121A011102)

摘　　要：目的:探讨冬凌草甲素(oridonin,Ori)干预前后,DC-CIK细胞对人多发性骨髓瘤RPMI 8226细胞杀伤活性的改变。方法:分离健康人外周血单个核细胞,诱导为DC-CIK细胞,LDH释放法检测DC-CIK细胞对药物作用前后RPMI 8226细胞的杀伤活性,流式细胞术检测药物作用下肿瘤细胞表面NKG2D配体的改变情况。结果:外周血单个核细胞成功诱导生成DC-CIK细胞;在相同效靶比时,Ori能明显提高DC-CIK细胞对肿瘤细胞的杀伤活性(P<0.01);流式检测结果显示,Ori作用后,RPMI8226细胞NKG2D配体ULBP1的表达增加最为显著(9.19±1.85)(15.47±0.67),(P<0.01);相关分析提示杀伤活性与ULBP1变化呈正相关(P<0.05)。结论:Ori能提升DC-CIK细胞对人多发性骨髓瘤RPMI 8226细胞的杀伤活性,可能与上调肿瘤细胞表面NKG2D配体的表达有关。Objective To investigate the changes in cytotoxicity of DC-CIK cells to human multiple myeloma RPMI 8226 cells before and after treatment with oridonin. Methods Normal human peripheral blood mononuclear cells were isolated and induced to obtain DC-CIK cells. Cytotoxicity of DC-CIK cells against RPMI 8226 cells which were treated by oridonin was analyzed by LDH releasing assay. The variation for expression of NKG2D ligands on RPMI 8226 cells were measured by flow cytometry. Results DC-CIK cells were successfully induced from the peripheral blood mononuclear cells. At the same effector to target ratio, oridonin obviously enhanced the cytotocixity of DC-CIK cells against RPMI 8226 cells （P〈0.01）. Flow cytometry showed the expression of NKG2D ligands ULBP1 of RPMI8226 cells was most significantly increased as the cells were treated by oridonin [（9.19 ± 1.85） vs. （15.47 ± 0.67）, P〈0.01]. Correlation analysis indicated that cytotocixity was positively correlated with changes in ULBP1. Conclusions Oridonin can improve the cytotoxicity of DC-CIK cells against RPMI 8226 cells, which may be related with the increased expressions of NKG2D ligands on the tumor cell surface.

关 键 词：冬凌草甲素 多发性骨髓瘤 NKG2D-NKG2D配体 

分 类 号：R733.3[医药卫生—肿瘤]