Hydrogen sulfide protects retina from blue light-induced photodamage and degeneration via inhibiting ROS-mediated ER stress-CHOP apoptosis signal

ABSTRACT

Background: Hydrogen sulfide (H₂S) is a small reducing gas molecule with various biological functions such as anti-oxidative, anti-apoptotic and anti-inflammatory activities. In this study, we investigated the therapeutic effects of exogenous H₂S in the experimental models of retinal photodamage in vivo and in vitro.

Methods: Rats with open eyelids were pretreated with H₂S (80~120 μmol/kg) for 10 days and then continuously exposed to blue light (435~445nm, 11.2W/m2) for 8 h to establish in vivo experimental model. ARPE-19 cells were pretreated with H₂S and then exposed to blue light to establish in vitro experimental model.

Results: In vivo experiments, H₂S significantly ameliorated blue light-induced retinal oxidative stress, apoptosis and degeneration. Moreover, H₂S inhibited the activation of blue light-induced endoplasmic reticulum (ER) stress CHOP apoptotic signaling. In vitro experiments, H₂S improved blue light-induced oxidative stress and oxidative damage. H₂S inhibited ROS-mediated activation of ER stress CHOP apoptotic signaling. H₂S alleviated blue light-induced apoptosis and increases cell viability. The ER stress inhibitor 4-PBA alleviated blue light-induced apoptosis and increases cell viability.

Conclusion: Taken together, these results indicate that H₂S can inhibit ROS-mediated ER stress-CHOP apoptosis signal, thereby alleviating blue light-triggered retinal apoptosis and degeneration.

KEYWORDS:

• H₂S
• photodamage
• retinal degeneration
• oxidative damage
• endoplasmic reticulum stress
• reactive oxygen species‌
• apoptosis
• ARPE-19 cells

Acknowledgements

The authors are grateful to the Core Facility of School of Life Sciences, Lanzhou University. This work is supported partly by the LZU-IMPCAS cooperation.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Availability of data and materials

The data used to support the findings of this study are available from the corresponding author upon request.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.