摘要
目的研究不同浓度紫杉醇作用人肺腺癌A549细胞48小时后NKG2D配体表达的改变及CIK细胞杀伤活性的变化。方法 采用MTT法测定紫杉醇对A549细胞24小时的50%抑制率(IC50);流式细胞术检测IC50、1/2 IC50、1/4 IC50浓度紫杉醇作用A549细胞48小时后A549细胞表面NKG2D配体(MICA、MICB、ULBP1、ULBP2、ULBP3)表达的变化;乳酸脱氢酶释放法检测不同效靶比时,CIK细胞对IC50浓度的紫杉醇作用前及作用48小时后A549细胞的杀伤活性。结果 不同浓度紫杉醇作用48小时后A549细胞表面MICA、MICB、ULBP2、ULBP3表达显著升高,ULBP1表达降低(P<0.05)。效靶比10∶1、20∶1、30∶1时,CIK细胞对A549细胞的杀伤活性分别为(11.08±1.22)%、(36.22±0.91)%、(45.73±2.00)%;CIK细胞对IC50浓度紫杉醇作用48小时后的A549细胞杀伤活性分别为(20.79±3.33)%,(53.47±1.62)%、(66.39±0.77)%,与作用前比较均明显增强(P<0.05)。结论 紫杉醇作用后能提高A549细胞NKG2D配体(MICA、MICB、ULBP2、ULBP3)的表达,从而增强A549细胞对CIK细胞杀伤的敏感性。
Objective To analyze the effects of paclitaxel on the expression of NKG2D ligands and the cytotoxicity of cytokineinduced killer（CIK） cells against human lung adenocarcinoma cell line A549 after 48 hours treated with different concentrations of paclitaxel. Methods The IC50 of paclitaxel against A549 cells was measured by MTY assay. The expression of NKG2D ligands（ MICA, MICB ,ULBP1 ,ULBP2, ULBP3 ） on surface of A549 cell before and after 48 hours treated by paclitaxel（ IC50,1/2 IC50, 1/4 IC50 ） was assaied by flow cytometery. Cytotoxicities of CIK cells against A549 cells before and after 48 hours cultured by ICso paclitaxel were analyzed by LDH releasing assay at effector-to-target cell ratio（E： T） of 10： 1,20： 1,30： 1. Results Expression of NKG2D ligands （ MICA, MICB, ULBP2, ULBP3 ） on A549 cells was up-expressed after cultured with different concentrations of paclitaxel for 48 hours, while ULBP1 was decreased（P 〈 0.05 ）. Cytotoxicity of CIK cells against A549 cells was （ 11.08 ± 1.22） % , （ 36.22 ± 0.91 ） % , （45.73 ± 2.00） % at the E ： T ratios of 10 ： 1,20 ： 1,30 ： 1, respectively, which was significantly increased after treated with ICso paclitaxel（ P 〈 0. 05 ）. Conclusion Pachtaxel can up-regulate the expressions of MICA, MICB, ULBP2, ULBP3, which enhances the susceptibility of A549 cells to the CIK cell mediated lysis.
出处
《实用肿瘤杂志》
CAS
2013年第1期49-52,共4页
Journal of Practical Oncology
基金
郑州市科技领军人才项目(121PLJRC532)
