本文通过体外细胞实验应用6-姜烯酚对HCT116和HT29进行干预，以探讨6-姜烯酚诱导结直肠癌细胞凋亡及与相关凋亡蛋白（Bax、BCL2、Caspase3和PARP1）表达之间的关系。利用倒置荧光显微镜观察不同浓度的6-姜烯酚干预HCT116及HT29后细胞形态的变化，CCK8法测定不同分组HCT116及HT29抑制率，并绘制细胞增殖曲线，Annexin V-FITC/PI流式细胞术检测不同分组HCT116及HT29凋亡，Western-blot检测分析凋亡相关蛋白表达情况（Bax、BCL2、Caspase3和PARP1）。结果显示，与对照组相比，6-姜烯酚可不同程度地诱导HCT116及HT29凋亡，促进Bax、Caspase3和PARP1蛋白水平表达（p<0.05），抑制BCL2蛋白水平表达（p<0.05），并增加Bax/BCL2比值比例（p<0.05）。因此，6-姜烯酚诱导HCT116、HT29发生凋亡可能是与激活Bax、Caspase3和PARP1的表达以及增加Bax/BCL2比值比例相关，这一发现可为结直肠癌的临床治疗与预防提供有效参考依据。

In this study, HCT116 and HT29 were directly induced by 6-shogoal through in vitro cell experiment to investigate the effects of 6-shogoal on the apoptosis of human colorectal cancer cells and the expression of associated apoptotic proteins (Bax, BCL2, Caspase3 andPARP1). The changes of cell morphology with the treatment of 6-shogoal were observed by inverted phase contrast microscope. The inhibition rate of HCT116 and HT29 was detected by CCK8 and the cell proliferation curves were drawn.The apoptosis in human HCT116 and HT29 were detected by Annexin V-FITC/PI flow cytometr and the expression of related proteins (Bax, BCL2, Caspase3 and pARp1) was analyzed using western-blot). Compared with the model group, 6-shogoal could inhibit the apoptosis of HCT116 and HT29 in a concentration dependent manner (p<0.05), which also could enhance the expression of Bax, Caspase3 and PARP1 inhibit the expression of BCL2 and increase the ratio of Bax/BCL2 (p<0.05). Therefore, the apoptosis of HCT116 and HT29induced by 6-shogoalmay be related to the activation of Bax, Caspase3, PARP1 expression and the increase of the Bax/BCL2 ratio. This finding can provide references for the clinical treatment and prevention of colorectal cancer.

宁夏自然科学基金项目（NZ16136）；宁夏“研究生教育创新计划”学位点建设项目（YXW2017014）