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作 者:李芳[1] 洪昆[2] 黄瓅[3] 苏晓丽[3] 胡成平[3]
机构地区:[1]郑州大学第一附属医院呼吸与危重症医学科,河南郑州450000 [2]岳阳职业技术学院,湖南岳阳414000 [3]中南大学湘雅医院呼吸与危重症医学科,湖南长沙410008
出 处:《河南医学研究》2015年第6期1-5,共5页Henan Medical Research
摘 要:目的探讨氯化钴化学乏氧对人肺腺癌A549细胞生长及迁徙、侵袭能力的影响。方法采用氯化钴(CoCl2)建立人肺腺癌A549细胞体外化学乏氧模型。首先通过倒置相差显微镜、电镜、MTT法及流式细胞学观察CoCl2对A549细胞形态、增殖及细胞周期的影响;进一步利用Transwell小室模型检测CoCl2对A549细胞侵袭及迁徙能力的影响。结果与常氧对照组相比,200μmol/L CoCl2化学乏氧组A549细胞光镜下较稀疏,电镜下出现线粒体肿胀、内质网扩张及自噬泡形成等微观结构改变,生长曲线低平、增殖缓慢,G1期细胞比例增多、S期细胞比例减少;迁徙及侵袭能力增强。结论 CoCl2化学乏氧抑制人肺A549细胞的增殖,诱导G1/S周期阻滞,增强A549细胞的侵袭及迁徙能力。Objective To investigate the effect of CoCl2 induced chemical hypoxia on proliferation,invasion and migration in human lung adenocarcinoma A549 cells. Methods CoCl2 was utilized to establish chemical hypoxia model of human lung adeno-carcinoma A549 cells. First,inverted light and electron microscope,MTT assay and flow cytometry were used to observe the effect of CoCl2 on the morphology and structure,proliferation and cell cycle of A549 cells. Then,transwell booth model was used to de-tect the capability of cellular invasion and migration of A549 cells. Results Compared with control group,there were fewer cells and mitochondrial swelling,endoplasmic reticulum expansion and autophagic vacuoles in A549 cells of CoCl2 group,with low and flat growth curve,more G1 phase cells and less S phase cells,while the ability of migration and invasion were both increased. Conclusion CoCl2 induced chemical hypoxia inhibited cell proliferation,induced G1/S arrest,and enhanced the ability of inva-sion and migration in human lung A549 cell.
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