Can hydrogen therapy help prevent blindness in premature babies?

This study suggests hydrogen gas inhalation could help prevent retinopathy of prematurity (ROP), a leading cause of blindness in premature babies. The research showed hydrogen therapy promoted healthy eye blood vessel development while preventing harmful overgrowth.

How does hydrogen gas protect the eyes in retinopathy of prematurity?

Hydrogen works by activating the body's natural antioxidant defenses and regulating oxygen-sensing pathways. This helps promote healthy blood vessel regrowth while preventing the dangerous overgrowth that causes vision loss in ROP.

Is hydrogen therapy safer than current ROP treatments?

The study suggests hydrogen inhalation could be safer than current treatments like anti-VEGF injections and laser therapy, which can have complications. Hydrogen gas has no known toxic effects and works naturally with the body's protective systems.

What concentration of hydrogen gas was used in this study?

Researchers used hydrogen gas at 3-4% concentration for inhalation therapy. This concentration was effective at protecting eye blood vessels without interfering with normal development.

Has hydrogen therapy been tested in human babies with ROP?

This study was conducted in mice that develop a condition similar to human ROP. While the results are promising, human clinical trials would be needed to confirm safety and effectiveness in premature babies.

Hydrogen Gas Protects Premature Babies' Eyes from Blindness-Causing Disease

Authors: Yatu Guo, Jiahui Qin, Ruiqiang Sun, Peng Hao, Zhixin Jiang, Yuchuan Wang, Zhiqi Gao, Huan Zhang, Keliang Xie, Wei Zhang
Journal: Biological Research
Year: 2024
DOI: 10.1186/s40659-024-00515-z
Study Type: Mouse
Outcome: Positive
Peer Reviewed: Yes
Country: China
Health Condition: Retinopathy of Prematurity
Body System: Visual

TL;DR

Inhaling hydrogen gas helps reduce damage and improve healing in the eyes of mice with a disease similar to one that causes blindness in premature babies, without affecting normal eye development.

Key Finding

Inhaling 3-4% hydrogen gas promoted normal retinal blood vessel regeneration while suppressing abnormal blood vessel growth and protecting eye support cells in mice with oxygen-induced retinopathy.

Summary

This study examined whether inhaling molecular hydrogen gas could help treat retinopathy of prematurity (ROP), a serious eye disease in premature infants that can cause blindness. Researchers exposed newborn mice to high oxygen levels to mimic ROP, then gave some mice hydrogen gas to breathe. The hydrogen treatment helped restore normal blood vessel growth in the retina while reducing abnormal blood vessel growth and protecting supporting cells in the eye, likely by reducing harmful molecules called free radicals.

Practical Takeaway

This is early-stage research conducted only in mice, not humans. While the results are promising and suggest hydrogen inhalation may eventually help treat retinopathy of prematurity, much more research—including human clinical trials—would be needed before this could become a treatment option. Parents of premature infants should continue following current medical recommendations and discuss any interest in hydrogen therapy with their eye specialist.

Abstract

Background: Retinopathy of Prematurity (ROP) is a proliferative retinal vascular disease occurring in the retina of premature infants and is the main cause of childhood blindness. Nowadays anti-VEGF and retinal photocoagulation are mainstream treatments for ROP, but they develop a variety of complications. Hydrogen (H2) is widely considered as a useful neuroprotective and antioxidative therapeutic method for hypoxic-ischemic disease without toxic effects. However, whether H2 provides physiological angiogenesis promotion, neovascularization suppression and glial protection in the progression of ROP is largely unknown.This study aims to investigate the effects of H2 on retinal angiogenesis, neovascularization and neuroglial dysfunction in the retinas of oxygen-induced retinopathy (OIR) mice. Methods: In this study, mice that were seven days old and either wild-type (WT) or Nrf2-deficient (Nrf2-/-) were exposed to 75% oxygen for 5 days and then returned to normal air conditions. Different stages of hydrogen gas (H2) inhalation were administered. Vascular obliteration, neovascularization, and blood vessel leakage were analyzed and compared. To count the number of neovascularization endothelial nuclei, routine HE staining of retinal sections was conducted. Immunohistochemistry was performed using DyLight 594 labeled GSL I-isolectin B4 (IB4), as well as primary antibodies against proliferating cell nuclear antigen (PCNA), glial fibrillary acidic protein (GFAP), and Iba-1. Western blots were used to measure the expression of NF-E2-related factor 2 (Nrf2), vascular endothelial growth factor (VEGF), Notch1, Dll4, and HIF-1α. Additionally, the expression of target genes such as NQO1, HO-1, Notch1, Hey1, Hey2, and Dll4 was measured. Human umbilical vein endothelial cells (HUVECs) treated with H2 under hypoxia were used as an in vitro model. RT-PCR was used to evaluate the mRNA expression of Nrf2, Notch/Dll4, and the target genes. The expression of reactive oxygen species (ROS) was observed using immunofluorescence staining. Results: Our results indicate that 3-4% H2 does not disturb retinal physiological angiogenesis, but ameliorates vaso-obliteration and neovascularization in OIR mice. Moreover, H2 prevents the decreased density and reverses the morphologic and functional changes in retinal astrocytes caused by oxygen-induced injury. In addition, H2 inhalation reduces microglial activation, especially in the area of neovascularization in OIR mice. H2 plays a protective role in vascular regeneration by promoting Nrf2 activation and suppressing the Dll4-induced Notch signaling pathway in vivo. Also, H2 promotes the proliferation of HUVECs under hypoxia by negatively regulating the Dll4/Notch pathway and reducing ROS levels through Nrf2 pathway aligning with our findings in vivo.Moreover, the retinal oxygen-sensing mechanisms (HIF-1α/VEGF) are also involved in hydrogen-mediated retinal revascularization and neovascularization suppression. Conclusions: Collectively, our results indicate that H2 could be a promising therapeutic agent for POR treatment and that its beneficial effect in human ROP might involve the activation of the Nrf2-Notch axis as well as HIF-1α/VEGF pathways.