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分子氢治疗角膜 UVB 诱导的氧化应激和光损伤的疗效。

Therapeutic effect of molecular hydrogen in corneal UVB-induced oxidative stress and corneal photodamage.

机构信息

Institute of Experimental Medicine of the Czech Academy of Sciences, 14220, Prague 4, Czech Republic.

Faculty of Natural Science, Charles University, Vinicna 7, 12843, Prague 2, Czech Republic.

出版信息

Sci Rep. 2017 Dec 21;7(1):18017. doi: 10.1038/s41598-017-18334-6.

DOI:10.1038/s41598-017-18334-6
PMID:29269749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5740126/
Abstract

The aim of this study is to examine whether molecular hydrogen (H) is able to reduce oxidative stress after corneal damage induced by UVB irradiation. We previously found that UVB irradiation of the cornea caused the imbalance between the antioxidant and prooxidant enzymes in the corneal epithelium, followed by the imbalance between metalloproteinases and their physiological inhibitors (imbalances in favour of prooxidants and metalloproteinases) contributing to oxidative stress and development of the intracorneal inflammation. Here we investigate the effect of H dissolved in PBS in the concentration 0.5 ppm wt/vol, applied on rabbit corneas during UVB irradiation and healing (UVB doses 1.01 J/cm once daily for four days). Some irradiated corneas remained untreated or buffer treated. In these corneas the oxidative stress appeared, followed by the excessive inflammation. Malondiladehyde and peroxynitrite expressions were present. The corneas healed with scar formation and neovascularization. In contrast, in H treated irradiated corneas oxidative stress was suppressed and malondiladehyde and peroxynitrite expressions were absent. The corneas healed with the restoration of transparency. The study provides the first evidence of the role of H in prevention of oxidative and nitrosative stress in UVB irradiated corneas, which may represent a novel prophylactic approach to corneal photodamage.

摘要

本研究旨在探讨分子氢(H)是否能减轻 UVB 照射诱导的角膜损伤后的氧化应激。我们之前发现,UVB 照射角膜会导致角膜上皮中抗氧化酶和促氧化剂酶之间的失衡,随后金属蛋白酶及其生理抑制剂之间的失衡(有利于促氧化剂和金属蛋白酶)导致氧化应激和角膜内炎症的发展。在这里,我们研究了浓度为 0.5 ppmwt/vol 的 H 在 PBS 中溶解后,在 UVB 照射和愈合期间(每天一次照射 1.01J/cm 的 UVB 剂量,持续四天)应用于兔角膜的效果。一些照射的角膜未经处理或缓冲液处理。在这些角膜中出现了氧化应激,随后出现了过度的炎症。丙二醛和过氧亚硝酸盐的表达存在。角膜愈合形成瘢痕和新生血管。相比之下,在 H 处理的照射角膜中,氧化应激受到抑制,丙二醛和过氧亚硝酸盐的表达不存在。角膜透明性恢复愈合。该研究首次提供了 H 在预防 UVB 照射角膜氧化和硝化应激中的作用的证据,这可能代表一种预防角膜光损伤的新方法。

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