T Yokota, N Kamimura, T Igarashi, H Takahashi, S Ohta, H Oharazawa
Clinical & Experimental Ophthalmology, 2015•Wiley Online Library
Background
Oxidative and nitrative processes have an important role in the pathogenesis of glaucomatous neurodegeneration. Oxidative stress occurs when cellular production of reactive oxygen species outweighs the protective capacity of antioxidant defences. Reactive oxygen species are generated as by‐products of cellular metabolism, primarily in the mitochondria. Herein, we present a novel investigation of the effects of molecular hydrogen (H2) on retinal cells exposed to oxidative stress.
Methods
We cultured adult rat retinal tissues in an organotypic culture system with a nitric oxide donor, S‐nitroso‐N‐acetylpenicillamine, in the presence or absence of H2. Loss of mitochondrial membrane potential and apoptosis of retinal cells were analysed using a MitoTMRE detection kit and TdT‐mediated dUTP nick end labeling (TUNEL) assay, respectively. Tyrosine nitration levels and oxidative stress damage in the retina were evaluated using immunohistochemical staining. Retinal damage was quantified by measuring the numbers of cells in the ganglion cell and inner nuclear layers and the thickness of the retina.
Results
H2 suppressed loss of mitochondrial membrane potential and apoptosis in retinal cells. Moreover, H2 decreased the tyrosine nitration level and suppressed oxidative stress damage in retinal cells. S‐nitroso‐N‐acetylpenicillamine treatment decreased the cell numbers in the ganglion cell layer and inner nuclear layer, but the presence of H2 inhibited this reduction. These findings suggest that H2 has a neuroprotective effect against retinal cell oxidative damage, presumably by scavenging peroxynitrite.
Conclusions
H2 reduces cellular peroxynitrite, a highly toxic reactive nitrogen species. Thus, H2 may be an effective and novel clinical tool for treating glaucoma and other oxidative stress‐related diseases.
分子氢对大鼠视网膜中一氧化氮衍生的过氧亚硝酸盐引起的氧化应激的保护作用
T Yokota、N Kamimura、T Igarashi、H Takahashi、S Ohta、H Oharazawa
临床与实验眼科学，2015•威利在线图书馆
——背 景
氧化和硝化过程在青光眼神经变性的发病机制中起着重要作用。当细胞产生的活性氧超过抗氧化防御的保护能力时，就会发生氧化应激。活性氧是细胞代谢的副产物，主要在线粒体中产生。在此，我们提出了一项关于分子氢 (H2) 对暴露于氧化应激的视网膜细胞影响的新研究。
——方 法
我们在有或没有 H2 的情况下，在含有一氧化氮供体 S-亚硝基-N-乙酰青霉胺的器官型培养系统中培养成年大鼠视网膜组织。分别使用 MitoTMRE 检测试剂盒和 TdT 介导的 dUTP 缺口末端标记 (TUNEL) 检测法分析线粒体膜电位的丧失和视网膜细胞的凋亡。使用免疫组织化学染色评估视网膜中的酪氨酸硝化水平和氧化应激损伤。通过测量神经节细胞和内核层中的细胞数量以及视网膜厚度来量化视网膜损伤。
——结 果
H2 抑制了视网膜细胞线粒体膜电位的丧失和细胞凋亡。此外，H2 降低了酪氨酸硝化水平并抑制了视网膜细胞的氧化应激损伤。S-亚硝基-N-乙酰青霉胺治疗减少了神经节细胞层和内核层中的细胞数量，但 H2 的存在抑制了这种减少。这些发现表明 H2 对视网膜细胞氧化损伤具有神经保护作用，大概是通过清除过氧亚硝酸盐来实现的。
——结 论
H2 降低了细胞过氧亚硝酸盐，这是一种毒性极强的活性氮物质。因此，H2 可能是治疗青光眼和其他氧化应激相关疾病的有效和新颖的临床工具。
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本文内容转载自临床与实验眼科学，2015•威利在线图书馆
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