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医学论文范文:外源磷脂酰乙醇胺诱导人宫颈癌HeLa细胞凋亡的研究
【摘要】 目的 磷脂酰乙醇胺(phosphatidylethanolamine, PE)在细胞凋亡的早期由细胞膜内侧翻转到外侧，与磷脂酰丝氨酸共同成为细胞凋亡的早期信号，但是其在凋亡中的作用尚不清楚。本研究探讨了PE对HeLa细胞凋亡的影响。方法 实验以人宫颈癌HeLa细胞系为材料，分别设置了空白对照组、0.125、0.25、0.5和1mmol/L PE处理组。以MTT检测细胞生长情况，PI流式细胞仪法检测细胞周期，Annexin VPI法检测细胞凋亡。结果 与对照组相比，PE各处理组对HeLa细胞生长的抑制作用呈剂量与时间依赖性，并诱导细胞凋亡发生，但不影响细胞周期。结论 PE通过诱导细胞凋亡而抑制HeLa细胞的生长。
【关键词】 磷脂酰乙醇胺;细胞凋亡;HeLa细胞
Apoptosis of human cervical cancer HeLa cells induced
by phosphatidylethanolamine
WANG Aiying, HU Xiaoyan, LI Zongfang,LIU Liying, NI Lei, YU Lin, SONG Tusheng
1. Key Laboratory of Environment and Genes Related to Diseases of Ministry ofEducation/ Genetics and Molecular Biology Department, Medical School ofXian Jiaotong University, Xian 710061; 2. the Second Affiliated Hospital,
Medical School of Xian Jiaotong Universitry, Xian 710004, China医.学全.在.线www.med126.com
ABSTRACT: Objective Phosphatidylethanolamine (PE) is an important phospholipid component in the cell membrane and is involved in the formation of membrane asymmetry. PE is exposed on the cell surface with phosphatidylserine during apoptosis. However, the effects of PE on cell apoptosis are not clear. In this study, we investigated effects of PE on apoptosis in human cervical cancer HeLa cells. Methods HeLa cells were used as the experiment material, and were divided into five groups: blank control group, and four treatment groups of 0.125, 0.25, 0.5 and 1 mmol/L PE, respectively. The cell growth was tested by MTT assay; the cell cycle and apoptosis were analyzed using flow cytometry. Results Compared with the control group, PE inhibited the growth of HeLa cells in all the treatment groups in dose and timedependent manners, and induced the apoptosis, but did not change the cell cycle. Conclusion PE inhibits the growth of HeLa cells by inducing the apoptosis.
KEY WORDS: phosphatidylethanolamine; apoptosis; HeLa cell
细胞膜的磷脂成分包括磷脂酰胆碱(phosphatidylcholine, PC)、磷脂酰乙醇胺(phosphatidylethanolamine, PE)、磷脂酰丝氨酸(phosphatidylserine, PS)和鞘磷脂(sphingomyelin, SM)[1]。在细胞膜上，磷脂呈不均等对称分布，PC和SM分布于细胞膜的外侧，而PE和PS分布于内侧[23]。氨基磷脂转位酶(aminophospholipid translocase)参与了PE和PS的膜不对称分布[4]。在正常情况下，氨基磷脂转位酶可以将细胞膜外侧的PE和PS转为内侧。抑制氨基磷脂转位酶活性可以诱导CNS衍化HN25和HOG细胞凋亡，并引起caspase3激活[5]，提示细胞膜磷脂分布异常可以引起细胞凋亡发生。细胞膜PS外翻已经成为细胞凋亡的重要检测指标，并有研究证明PS外翻参与了细胞凋亡的诱导过程[67]。在细胞凋亡过程中，PE也发生外翻作用，并与PS一起参与了凋亡细胞脂筏的形成[8]。近年研究发现细胞内PE结合蛋白(Raf kinase inhibitor protein, RKIP)表达增高，可以抑制RafERK1/2通路[9]。但是，关于PE是否能引起细胞增殖或凋亡尚不清晰，本研究组研究发现外源PE可以诱导宫颈癌HeLa细胞凋亡发生，现报道如下。
1 材料与方法
1.1 主要试剂及材料
RPMI 1640培养液和FBS胎牛血清购自GIBCO公司;PE和PI购自Sigma公司;Annexin VFITC apoptosis detection kit购自BD Bioscience公司。
