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机构地区:[1]成都市妇女儿童中心医院,四川成都610091 [2]自贡高新医院,四川自贡643000
出 处:《华西药学杂志》2017年第6期603-606,共4页West China Journal of Pharmaceutical Sciences
摘 要:目的研究大黄素促进结肠癌细胞自噬性凋亡的作用机制。方法通过MTT法及Hochest染色法来检测大黄素对结肠癌细胞增殖及凋亡的影响;用免疫荧光检测自噬体的形成,用免疫印迹法检测自噬相关标志性蛋白的表达、细胞凋亡相关标志蛋白p53及caspase-3的活化及表达情况;用流式细胞仪检测胞内活性氧(ROS)的表达。结果大黄素对结肠癌细胞具明显的抑制作用且呈浓度依赖性,并可诱发肿瘤细胞凋亡;大黄素可促进结肠癌细胞自噬体形成、诱发细胞自噬;还可激活胞内ROS的表达。自噬抑制剂氯喹及ROS抑制剂NAC均能显著诱发大黄素诱导的促凋亡蛋白caspase-3和p53的活化表达。结论大黄素通过促进结肠癌细胞胞内的ROS表达来激活细胞自噬,进而抑制结肠癌细胞的增殖。OBJECTIVE To study the mechanism of emodin on autophagy related - apoptosis in colon cancer cells. METHODS The proluferation and apoptosis of SW480 ceils were evaluated by MTT and Hoeehst staining. The marker proteins of autophagy and apoptosis in SW480 cells treated by emodin were detected by Immunofluoreseence and Western Blot. The relative reactive oxygen species(ROS) in cells treated by emodin were evaluated by flow cytometry. The expression of marker proteins of autophagy and apoptosis in cells treated by emodin and autophagy inhibitor chlorochine or ROS scavenger NAC were detected by Immunoblotting. RESULTS Emodin markedly inhibited cell proliferation and promoted cell apoptosis in a concertration dependent manner. The result of flow cytometry showed that emodin targeted the ROS of SW480 cells, and the results of Immunofluorescenee and Western Blot showed that emodin promoted SW480 cells autophagy reahed apoptosis by triggering ROS production. CONCLUSION Emodin may promote the autophagy related apoptosis of colon cells SW480 by increasing the production of ROS.
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