Hydrogen Therapy Protects Eye Cells from Chemical Damage in Rabbits
- Authors
- Runpu Li, Yingxin Qu, Xiaoqi Li, Ye Tao, Qinghua Yang, Junyi Wang, Yumei Diao, Qian Li, Yifan Fang, Yifei Huang, Liqiang Wang
- Journal
- Investigative Opthalmology & Visual Science
- Year
- 2021
- DOI
- 10.1167/iovs.62.9.2
- Study Type
- Rabbit
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Corneal Endothelial Decompensation
- Body System
- Ocular
TL;DR
Breathing molecular hydrogen (H2) gas can help heal and protect the cells on the back surface of the eye (corneal endothelial cells) from chemical damage.
Key Finding
Molecular hydrogen applied as hydrogen-rich saline reduced corneal endothelial cell death and improved cell function in rabbit and laboratory models of MNU-induced injury by decreasing oxidative stress and activating anti-death cellular pathways.
Summary
Researchers used rabbits and laboratory cell cultures to test whether molecular hydrogen (H2)—hydrogen gas dissolved in salt water—could protect corneal endothelial cells (the innermost layer of the eye's cornea) from damage caused by a toxic chemical called MNU. They found that hydrogen-rich saline reduced cell death, improved cell function, and decreased harmful oxidative stress (cellular damage from unstable molecules) by affecting specific cellular pathways involved in inflammation and cell survival.
Practical Takeaway
This early-stage animal study suggests hydrogen water or hydrogen-rich saline may have potential to protect eye cells from certain types of damage, but the research is limited to laboratory and rabbit models—not human studies. Much more research, including human trials, would be needed before any therapeutic claims could be made about hydrogen for eye health.
Abstract
Purpose: Previous work by our group has demonstrated the value of N-methyl-N-nitrosourea (MNU)-induced corneal endothelial decompensation in animal models. The aim of this study was to investigate the effect of molecular hydrogen (H2) on MNU-induced corneal endothelial cell (CEC) injury and the underlying mechanism. Methods: MNU-induced animal models of CEC injury were washed with hydrogen-rich saline (HRS) for 14 days. Immunofluorescence staining, immunohistochemical staining, and corneal endothelial assessment were applied to determine architectural and cellular changes on the corneal endothelium following HRS treatment. MNU-induced cell models of CEC injury were co-cultured with H2. The effect of H2 was examined using morphological and functional assays. Results: It was shown that MNU could inhibit the proliferation and specific physiological functions of CECs by increasing apoptosis and decreasing the expression of ZO-1 and Na+/K+-ATPase, whereas H2 improved the proliferation and physiological function of CECs by anti-apoptosis. Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-κB/NLRP3 pathway and the FOXO3a/p53/p21 pathway. Conclusions: This study suggests that topical application of H2 could protect CECs against corneal damage factors through anti-apoptotic effect, reduce the incidence and severity of corneal endothelial decompensation, and maintain corneal transparency.