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作 者:王希莹[1] 杨宏宽[2] 葛红岩[1] 白洁[1] 唐先玲[1] 关立南[1] 田霈[1] 刘平[1]
机构地区:[1]哈尔滨医科大学附属第一医院眼科,黑龙江哈尔滨150001 [2]哈尔滨医科大学附属第一医院神经外科,黑龙江哈尔滨150001
出 处:《哈尔滨医科大学学报》2014年第2期101-105,共5页Journal of Harbin Medical University
基 金:国家自然科学基金资助项目(30973275)
摘 要:目的探讨年龄相关性黄斑变性(AMD)患者视网膜内线粒体铁蛋白(FtMt)表达增加的原因,以及FtMt在AMD病理生理过程中的功能。方法应用蛋白质免疫印迹和实时定量PCR检测由双氧水(H2O2)和铁在ARPE细胞系诱导的FtMt核酸及蛋白表达。应用MTT法和流式细胞仪技术分别检测氧化应激对FtMt过表达和FtMt表达抑制的ARPE细胞系的细胞杀伤和凋亡影响。结果氧化应激而不是铁,在AMD中诱导FtMt表达增加。FtMt过表达和表达抑制在ARPE细胞分别起到对抗抑制和促进氧化应激引起的细胞损伤和细胞凋亡。结论 AMD患者视网膜中表达增高的FtMt表达可能是由累积的氧化应激水平引起的,而增高的FtMt在AMD可能进一步起到抗氧化应激损伤的作用。Objective To investigate the possible cause of the mitochondrial ferritin (FtMt) induction and the role of FtMt in the pathogenesis of age-related macular degeneration (AMD) in vitro. Methods Western blot and Real-time PCR were used to detect the mRNA and protein inductions of FtMt in ARPE cell line. Hydrogen peroxide-induced cell death and apoptosis in both FtMt-overexpressing and FtMt knockdown ARPE cell line were measured by MTT assay and flow cytometry, respectively. Results Oxidative stress, not iron induced increased expression of mRNA and protein of FtMt in ARPE cell line. Overexpression of FtMt attenuated H2O2 -induced cell death and apoptosis, but FtMt knockdown increased the cell death and apoptosis in ARPE cell line. Conclusion The accumulated oxidative stress level, rather than iron in the retina of AMD may cause the induction of FtMt. The increased FtMt may play a protective role against oxidative stress in AMD.
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