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

作者简介: 孙园园(1992-),女,2015级在读硕士研究生,研究方向为白内障及屈光不正,E-mail:yankesyybs@163.com.

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)


中图分类号: X171.5

Zinc Oxide Nanoparticles Inhibit the Expression and Activity of MnSOD in Murine Photoreceptor Cells in Vitro

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

CLC number: X171.5

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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。
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

Abstract: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.
Key words:zinc oxide nanoparticle/
murine photoreceptor cell/
mitochondrion/
reactive oxygen species/
manganese superoxide dismutase.