Abstract

BackgroundOxidative stress (OS) is an essential factor in the pathogenesis of branch retinal vein occlusion (BRVO). Studies have demonstrated the role of hydrogen gas in the regulation of OS. This study was designed to evaluate the efficacy of hydrogen gas on the BRVO rat model.MethodsTwenty-four BRVO rats were randomly divided into two groups: the hydrogen gas (H) group (42% H2, 21% O2, 37% N2) and the model (M) group (21% O2, 79% N2). Rats in the H group inhaled hydrogen gas for 8 h every day up to 30 d post-occlusion. Twelve age-matched healthy rats served as the control (C) group. Retinal function and morphology were detected at 1, 7, 14 and 30 d post-occlusion. Furthermore, the expression of vascular endothelial growth factor (VEGF-α) was detected by immunofluorescent staining.ResultsFull-field electroretinography (ffERG) revealed that the amplitude of the b-wave (dark-adaptation 3.0 response), the amplitude of the OPs2 wave and the light-adapted flicker response in the H group were all higher than those in the M group at 7 d post-occlusion (all p < 0.05). The reopen time of occlusive retinal vessels in the H group was 2.235 ± 1.128 d, which was shorter than that in the M group (4.234 ± 2.236 d, p < 0.05). The rats in the H group had a thinner IPL + GCL + NFL and an increased total retina compared with those in the M group at 3 d post-occlusion (p < 0.05), while the rats in the H group had a thicker INL, IPL + GCL + NFL and total retina compared with those at 7, 14 and 30 d post-occlusion (p < 0.05). Moreover, the flow velocity of ear vein blood was increased in the H group compared with that in the M group (p < 0.05). The expression of VEGF-α in the H group was dramatically decreased compared with that in the M group at 1, 7 and 14 d post-occlusion (p < 0.05), while the expression kept in similar level at 30 d post-occlusion (p > 0.05).ConclusionsOur findings demonstrate that inhalation of hydrogen gas could alleviate retinal oedema, shorten reopen time and improve retinal function, and the potential mechanism might be related to a decrease in VEGF-α expression.

Highlights

  • Oxidative stress (OS) is an essential factor in the pathogenesis of branch retinal vein occlusion (BRVO)

  • BRVO rat model The BRVO model was confirmed by OCT and fundus photography

  • 24 BRVO rats were randomly divided into 2 groups: the hydrogen gas (H) group (n = 12) and the model (M) group (n = 12)

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Summary

Introduction

Oxidative stress (OS) is an essential factor in the pathogenesis of branch retinal vein occlusion (BRVO). Studies have demonstrated the role of hydrogen gas in the regulation of OS. This study was designed to evaluate the efficacy of hydrogen gas on the BRVO rat model. Retinal vein occlusion (RVO) is mainly classified with central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO) according to the occlusive vein sites. First-line therapeutic methods include glucocorticoid, anti-VEGF, laser photocoagulation, and traditional herb medicines (mostly in eastern countries) [4]. Those treatment methods cannot meet the needs of some individuals. Glucocorticoid is convenient but inevitably produces various adverse side effects, such as increased susceptibility to infection, damage to the optic nerve, cataracts, and so on [5,6,7]. It is urgent to explore effective measures against BRVO with evident therapeutic effects and fewer adverse side effects

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