丁酸钠抑制淋巴因子激活杀伤细胞杀瘤活性的研究

目的：探讨低浓度丁酸钠(sodium butyrate)对人结肠腺癌细胞SW1116表面细胞间黏附分子-1(ICAM-1)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ICAM-1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ICAM-1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ICAM-1同时增加CEA的表达，从而改变效／靶细胞的结合有关。

Sodium butyrate inhibits the cytotoxic activity of LAK by modulating adhesion molecule expression on human colon cancer cells

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.