Hydrogen Water Protects Against Vision Loss in Retinitis Pigmentosa
- Authors
- Wei-Ming Yan, Tao Chen, Xiao-Cheng Wang, Lin-Song Qi, Guan-Hua Zhao, Guo-Qing Yang, Yi-Fei Ma, Ye Tao, Lei Zhang, Zuo-Ming Zhang
- Journal
- International Journal of Ophthalmology
- Year
- 2017
- DOI
- 10.18240/ijo.2017.10.03
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Retinitis Pigmentosa
- Body System
- Visual
TL;DR
Hydrogen-rich saline (HRS) helps protect the eyes from damage and controls immune cell activation in a rat model of retinitis pigmentosa, a degenerative eye disease.
Key Finding
Hydrogen-rich saline preserved retinal function and reduced photoreceptor degeneration in rats with induced retinitis pigmentosa, while controlling immune cell activation and increasing protective protein expression.
Summary
Researchers tested hydrogen-rich saline (a salt solution containing dissolved hydrogen gas) in rats with an induced eye disease that damages light-sensing cells in the retina. The treatment preserved vision function and reduced damage to photoreceptor cells (the cells that detect light). The hydrogen-rich saline appeared to work by controlling immune cell activity in the eye and increasing levels of a protective protein called Sirt1.
Practical Takeaway
This is an early-stage animal study showing hydrogen-rich saline may have potential for retinal diseases, but it was conducted only in rats and did not test the treatment in humans. Much more research, including human clinical trials, would be needed before any conclusions could be drawn about its usefulness for people with eye disease.
Abstract
Aim: To investigate the effects of hydrogen-rich saline (HRS) on microglia activation and Sirtuin type 1 (Sirt1) in rats with N-methyl-N-nitrosourea (MNU)-induced retinitis pigmentosa (RP). Methods: Rats were divided into norm (N) group, model (M) group and HRS (H) group. Rats in M and H groups were given saline and HRS respectively prior to and after administration of MNU. At one day (d1) and d3 afterwards, electroretinogram and histological examination were performed to confirm the effects of HRS on retinal function and structure of MNU-induced RP. Immunofluorescence staining of anti-ionized calcium-binding adapter molecule 1 (Iba1), a maker of microglia cells, was performed, with quantitative real-time polymerase chain reaction (qRT-PCR) for its mRNA quantification. Moreover, Sirt1 mRNA and protein expression in the retinas were detected by Western blot and qRT-PCR. Results: HRS preserved the retinal function and mitigated the reduction of photoreceptor degeneration in MNU-treated retinas. The presence of microglia cells was somewhat more obvious in H group than that in M group at d1. HRS suppressed the further activation of microglia cells, with the number of microglia cells less than that of M group at d3. Results of qRT-PCR of Iba1 were consistent with those of immunofluorescence staining, with the mRNA expression of Iba1 in H group more intensive than that of M group at d1 (P<0.05), while less than that of M group at d3 (P<0.05). Furthermore, the Sirt1 mRNA and protein expression decreased after MNU administration, while HRS mitigated the MNU-induced downregulation of Sirt1. Conclusion: HRS can effectively keep microglia activation induced by MNU to an appropriate extent, while upregulate Sirt1 in MNU-induced RP.