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目的 探讨5-烷基间苯二酚(5-alkylresorcinols,5ARs)诱导人结直肠癌细胞凋亡及与BCL2、Bax、PARP1和Caspase3表达的影响.方法 体外细胞实验应用5ARs直接对HT29、HCTll6进行干预诱导.利用倒置相差显微镜观察5ARs对HT29、HCT116干预后细胞形态的变化.CCK8法测定不同浓度5ARs诱导人HT29及HCT116抑制率.AnnexinV-FITC/PI流式细胞术检测5ARs诱导人HT29及HCTll6凋亡.Western-blot检测分析不同浓度5ARs诱导HT29及HCTll6后凋亡相关蛋白变化(BCL2、Bax、PARP1和Caspase3).结果 5ARs可呈浓度依赖性地抑制HT29及HCTll6增殖(P＜0.05);5ARs可诱导HT29及HCT116凋亡,并可增强Bax、PARP1和Caspase3表达,抑制BCL2表达,并提高Bax/BCL2的比值比例(P＜0.05).结论 5ARs可诱导HT29及HCT116凋亡,并且可能与激活Bax、PARP1和Caspase3表达及增加Bax/BCL2比值比例相关.“,”AIM To investigate the mechanism of 5-alkylresorcinols (5ARs)-induced apoptosis by detecting the effect on BCL2,Bax,PARP1 and Caspase3 expression patterns in colon cancer cell lines.METHODS After HT29 and HCT 116 cells were treated with different concentrations of 5ARs,cell morphological changes were observed by phasecontrast microscopy,cell proliferation and apoptosis phenotypes were evaluated by Cell Counting Kit-8 (CCK8) and Annexin V-FITC/PIflow cytometric assays,respectively,and the protein levels of BCL2,Bax,PARP1 and Caspase3 were detected by Western blotting assays.RESULTS CCK8 assays indicated that the proliferation of HT29 and HCT 116 cells treated with different concentrations of 5ARs was significantlydecreased (P ＜ 0.05),and treatment with 5ARsincreased the apoptosis of HT29 and HCT 116cells.5ARs suppressed BCL2 expression andelevated the levels of Bax,PARP1,Caspase3 andthe ratio of BAX to BCL2 in colon cancer cells.CONCLUSION 5ARs can induce the apoptosis of HT29 and HCT 116 cells in vitro,possibly by enhancing BAX,PARP1 and Caspase3 expression and elevating the ratio of BAX to BCL2 in colon cancer cells.