Hydrogen Gas Protects Eye Cells from Damage After Blood Flow Loss
- Authors
- Jiangchun Wu, Ruobing Wang, Dianxu Yang, Wenbin Tang, Zeli Chen, Qinglei Sun, Lin Liu, Rongyu Zang
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2018
- DOI
- 10.1016/j.bbrc.2017.12.146
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Retinal Ischemia/Reperfusion Injury
- Body System
- Visual System
TL;DR
Breathing in a mix of hydrogen and oxygen can protect the nerve cells in the eye and preserve vision after an eye injury that cuts off blood supply.
Key Finding
Inhaled hydrogen gas protected rat retinal cells from ischemia/reperfusion injury and preserved visual function by activating the PI3K/Akt cellular pathway, and blocking this pathway eliminated hydrogen's protective effects.
Summary
Researchers studied whether inhaled hydrogen gas could protect rat eyes from damage caused by temporary loss of blood flow followed by blood flow restoration (a condition called ischemia/reperfusion injury). Rats with this eye injury inhaled a mixture of hydrogen and oxygen for one hour daily for a week. The hydrogen treatment reduced cell death in the retina (the light-sensing tissue at the back of the eye) and preserved vision. The protection appeared to work by activating a specific cellular pathway called PI3K/Akt, which prevents cells from dying.
Practical Takeaway
This rat study provides early evidence that hydrogen gas may have potential for protecting eye tissue from ischemic damage, but it is a preliminary finding in animals only. Much more research, including human studies, would be needed to determine if inhaled hydrogen could help treat eye diseases in people. The specific mechanism identified (PI3K/Akt activation) may be important for understanding how hydrogen works, but this does not yet translate to clinical recommendations.
Abstract
Retinal ischemia/reperfusion injury (IRI) plays a crucial role in the pathophysiology of various ocular diseases. Our previous study have shown that postconditioning with inhaled hydrogen (H2) (HPC) can protect retinal ganglion cells (RGCs) in a rat model of retinal IRI. Our further study aims to investigate potential mechanisms underlying HPC-induced protection. Retinal IRI was performed on the right eyes of rats and was followed by inhalation of 67% H2 mixed with 33% oxygen immediately after ischemia for 1 h daily for one week. RGC density was counted using haematoxylin and eosin (HE) staining, retrograde labelling with cholera toxin beta (CTB) and TUNEL staining, respectively. Visual function was assessed using flash visual evoked potentials (FVEP) and pupillary light reflex (PLR). The phosphorylated Akt was analysed by RT-PCR and western blot. The results showed that administration of HPC significantly inhibited the apoptosis of RGCs and protected the visual function. Simultaneously, HPC treatment markedly increased the phosphorylations of Akt. Blockade of PI3K activity by inhibitors (LY294002) dramatically abolished its anti-apoptotic effect and lowered both visual function and Akt phosphorylation levels. Taken together, our results demonstrate that HPC appears to confer neuroprotection against retinal IRI via the PI3K/Akt pathway.