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机构地区:[1]南京大学医学院附属鼓楼医院消化内科,江苏南京210008
出 处:《医学研究生学报》2005年第5期393-396,共4页Journal of Medical Postgraduates
基 金:江苏省卫生厅医学科技发展基金资助项目(批准号:H200122)
摘 要:目的:探讨低浓度丁酸钠(sodiumbutyrate)对人结肠腺癌细胞SW1116表面细胞间黏附分子1(ICAM1)和癌胚抗原(CEA)表达的影响及其对淋巴因子激活杀伤(LAK)细胞杀伤活性的改变。方法:噻唑蓝(MTT)比色法检测经不同浓度丁酸钠处理4天后SW1116在不同效/靶比下对LAK细胞杀伤敏感性的改变,流式细胞术和免疫荧光法定量和定性检测丁酸钠对ICAM1和CEA表达的影响。结果:MTT显示,经0.5、1和2mmol/L丁酸钠处理后,细胞对LAK细胞杀伤敏感性从74.6%下降至15.9%(效/靶为20),且在一定程度上有浓度依赖性,当效/靶为10时亦呈类似变化,与之对应的ICAM1阳性细胞数从92.2%下降至7.6%,而CEA阳性细胞数从1.2%上升至16.6%,荧光显微镜下与流式细胞术的改变相一致。结论:丁酸钠减弱LAK细胞对人结肠癌细胞SW1116的杀伤,这种作用可能与其降低ICAM1同时增加CEA的表达,从而改变效/靶细胞的结合有关。Objective:To investigate whether the susceptibility of human colon adenocarcinoma cell SW1116 to lymphokine-activated killer cell (LAK)-mediated lysis could be enhanced by low concentration of sodium butyrate, and the possible involvement of intercellular surface adhesion molecule-1 (ICAM-1) and carcinoembryonic antigen (CEA). Methods:Standard MTT assay was used to evaluate the cytotoxic activity of LAK cells to SW1116 cells, flow cytometric and immunofluorescent techniques were used to determine the expression of ICAM-1 and CEA on tumor cells. Results:Treatment of SW1116 with sodium butyrate leads to an increased resistance to LAK-mediated lysis, accompanied by downregulation of ICAM-1 expression and upregulation of CEA expression. Conclusion: Sodium butyrate inhibits rather than enhance LAK activity against SW1116, probably by changing the expression of ICAM-1 and CEA on target cells, which impair the adherence of effector on target cells.
关 键 词:丁酸钠 结肠癌 淋巴因子激活杀伤细胞 细胞间黏附分子1 癌胚抗原
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