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孙园园1,郭大东2,刘滨1,丁红燕3,徐溢4,毕宏生2,*. ZnO纳米粒子抑制体外小鼠光感受器细胞MnSOD的表达及活性[J]. 生态毒理学报, 2017, 12(3): 747-754
ZnO纳米粒子抑制体外小鼠光感受器细胞MnSOD的表达及活性
Zinc Oxide Nanoparticles Inhibit the Expression and Activity of MnSOD in Murine Photoreceptor Cells in Vitro
投稿时间:2016-11-29  修订日期:2017-01-05
DOI:10.7524/AJE.1673-5897.20161129001
中文关键词:  氧化锌纳米粒子  小鼠光感受器细胞  线粒体  活性氧  锰超氧化物歧化酶
英文关键词:zinc oxide nanoparticle  murine photoreceptor cell  mitochondrion  reactive oxygen species  manganese superoxide dismutase
基金项目:江苏省介入医疗器械研究重点实验室开放基金课题资助项目(项目编号jr1602);山东省高校中医药抗病毒协同创新中心资助项目(项目编号:XTCX2014A04-04)
作者单位
孙园园1,郭大东2,刘滨1,丁红燕3,徐溢4,毕宏生2,* 1. 山东中医药大学第二临床医学院济南 250014 2. 山东中医药大学眼科研究所济南 250002 3. 淮阴工学院 江苏省介入医疗器械研究重点实验室淮安 223003 4. 山东大学临床医学院济南 250012 
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中文摘要:
      随着纳米技术的发展,纳米材料在生物医药以及化工中已得到广泛应用。作为一类新型材料,其安全性也日益受到人们的高度关注。为探索氧化锌(ZnO)纳米粒子对小鼠视网膜光感受器细胞的毒性作用,本文通过MTT、荧光染色、流式细胞术、实时荧光定量PCR和酶联免疫吸附试验(ELISA)等技术,分别对经不同浓度ZnO纳米粒子处理的小鼠光感受器细胞活性、活性氧水平、锰超氧化物歧化酶(MnSOD)的基因和蛋白表达及活性进行了检测。结果表明,ZnO纳米粒子可通过诱导细胞线粒体产生过多的活性氧,降低线粒体膜电位,导致小鼠视网膜光感受器细胞损伤;ZnO纳米粒子能显著减少MnSOD在mRNA和蛋白质水平的表达,降低MnSOD活性,加剧氧化应激介导的细胞损伤。因此,氧化应激水平的提高导致了过量的活性氧产生及MnSOD表达和活性的下降,与ZnO纳米粒子引起的细胞毒性作用有关。
  
AuthorAffiliation
Sun Yuanyuan1, Guo Dadong2, Liu Bin1, Ding Hongyan3, Xu Yi4, Bi Hongsheng2,*1. The Second Clinical Medical College of Shandong University of Traditional Chinese Medicine, Jinan 250014, China 2. Eye Institute of Shandong University of Traditional Chinese Medicine, Jinan 250002, China 3. Jiangsu Provincial Key Laboratory for Interventional Medical Devices, Huaiyin Institute of Technology, Huaian 223003, China 4. School of Clinical Medicine, Shandong University, Jinan 250012, China
英文摘要:
      Nanomaterials have been widely used in areas of biology, pharmacy and chemical industry due to its rapid development. As a new type of material, the toxicity of nanomaterials is also attracting enormous attention. In the present study, the effects of ZnO nanoparticles (NPs) on murine photoreceptor cell viability and on the expression and activity of MnSOD were investigated by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, fluorescent analysis, flow cytometry, quantitative real-time PCR and enzyme-linked immunosorbent assay (ELISA) techniques. ZnO NPs exhibited high cytotoxicity on the target cells in concentration- and time-dependent manners. ZnO NPs elevated intracellular levels of reactive oxygen species (ROS) and collapsed the mitochondrial membrane potential, thus leading to murine photoreceptor cell damage. Moreover, ZnO NPs significantly reduced the expression of MnSOD at both mRNA and protein levels, attenuated its activity, and further aggravated the oxidative stress-mediated cell damages. Overall, ZnO NPs-induced cytotoxicity on murine photoreceptor cells was closely associated with elevated levels of oxidative stress via the overproduction of ROS and decreased expression and activity of MnSOD.
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