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作 者:梁荔[1] 盛红光[1] 刘雯[2] 施宝民[1] 王金申[1] 姜言明[1] 张敏[1]
机构地区:[1]山东大学附属省立医院胃肠外科,山东济南250021 [2]山东大学附属省立医院病理科,山东济南250021
出 处:《中国现代普通外科进展》2009年第12期1026-1029,共4页Chinese Journal of Current Advances in General Surgery
摘 要:目的:探讨二十二碳六烯酸(DHA)对人胃癌细胞系SGC-7901的作用及对MAPKs信号转导通路中ERK1/2通路蛋白及凋亡蛋白caspase-3表达的影响。方法:采用MTT法及流式细胞仪技术对细胞增殖和凋亡进行观察和分析;应用Westernblot技术检测不同浓度的DHA诱导胃癌细胞的丝裂原活化蛋白激酶ERK1/2及其磷酸化水平的表达以及其下游通路中凋亡蛋白caspase-3的表达。结果:DHA对于SGC-7901胃癌细胞的增殖有明显抑制作用,呈现时间和浓度依赖性(P<0.01)。DHA可诱导SGC-7901细胞凋亡,凋亡率随DHA的作用浓度增加而增加(P<0.01)。ERK1/2在对照组和不同DHA浓度组稳定表达,且表达无差异;P-ERK1/2活性随DHA作用浓度的增高而降低,差异有统计学意义(P<0.05);caspase-3随着DHA浓度的增高表达不断增强,差异有统计学意义(P<0.05)。结论:DHA可能通过下调ERK1/2的磷酸化过程,激活凋亡蛋白caspase-3的表达,诱导胃癌细胞的凋亡。Objective: To investigate the effects of DHA-induced apoptosis of gastric cancer SGC-7901 cells and the role of ERK1/2 MAPKsignaling transduction pathway and the apoptosis protein caspase-3. Methods: The inhibitive effects of DHA on SGC-7901 cells were assessed with MTT assay. Apoptosis was evaluated by flow cytometry. The expressions of ERK1/2, p-ERK1/2 and caspase-3 protein were detected by Western blot. Results: DHA inhibited the proliferation of SGC-7901 cells in a time-and-dose-dependent manner and also induced the apoptosis of SGC-7901 cells. The protein of ERK1/2 was steadily expressed among control and each experimental groups and the protein expression of p-ERK1/2 decreased, whereas the activity of caspase-3 increased with the dose of DHA. Conclusion: DHA maybe impact the phosphorylation process of ERK1/2 and regulate the expression of the apoptosis protein caspase-3, which induces apoptosis in gastric cancer cells.
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