埃托米达能通过Nrf2/HO-1通路保护视网膜质细胞免受过氧化引起的损伤
Xuan Zhao1,2, De-Gang Fan3, Xin-Chao Zhang2,4
1Department of Histology and Embryology, School of Basic Medical Sciences, Xi'an Medical University, Xi'an 710021, Shaanxi Province, China.
International journal of ophthalmology
|September 19, 2024
概括
埃托米达 (ET) 通过减少氧化应激,保护视网膜性细胞 (RGC) 免受过氧化 (H2O2) 损伤. 这种神经保护作用包括抑制iNOS和增加Nrf2/HO-1等抗氧化途径.
科学领域:
- 神经科学是一个神经科学.
- 眼科医生 眼科 眼科
- 毒理学 毒理学 毒理学
背景情况:
- 视网膜质细胞 (RGCs) 容易受到氧化应激的影响,这是视神经病变的关键因素.
- 过氧化 (H2O2) 是一种常见的氧化应激诱导剂,导致RGC损伤和亡.
- 麻醉剂埃托米达 (ET) 正在研究其麻醉作用之外的潜在神经保护性质.
研究的目的:
- 评估埃托米达 (ET) 在RGC中对H2O2诱导的氧化应激的保护作用.
- 阐明ET在RGC中的潜在抗氧化机制.
- 在视网膜损伤的体内模型中评估ET的疗效.
主要方法:
- 主要的RGCs被培养并受到H2O2诱导的氧化应激.
- 在暴露于H2O2之前,细胞经过不同度的ET (1,5,10μmol/L) 的预处理.
- 评估了细胞活力,细胞亡,氧化,甲和谷氨水平.
- 基因和蛋白质表达的iNOS,Nrf2,HO-1,和谷氨过氧化酶1被分析使用qRT-PCR和西方布洛特.
- 一个体内视神经切割 (ONT) 模型被用来评估ET在视网膜组织中的影响.
主要成果:
- 埃托米达显著增加了RGC活力,以剂量依赖的方式,在10μmol/L时获得最大的保护.
- ET治疗减少了iNOS表达和H2O2诱导的RGC亡.
- ET在mRNA和蛋白质水平上对抗氧化因子Nrf2和HO-1的表达进行了上调.
- 西方斑点证实在ET治疗的RGC和视网膜中降低了iNOS和合烯蛋白水平,并增加了Nrf2和HO-1表达.
结论:
- 埃托米达对RGC产生显著的神经保护作用,防止H2O2引起的损伤.
- 神经保护通过ET的抗氧化特性进行介导,包括iNOS抑制和Nrf2/HO-1通路激活.
- ET有效降低氧化应激标志物,并增强RGC和视网膜组织中的抗氧化防御,表明治疗潜力.
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