# Pyrroloquinoline Quinone Protects Against Light-Induced Retinal Damage in Association with the Suppression of c-Fos Signalling

## TL;DR

Pyrroloquinoline quinone (PQQ) protects the retina from light-induced damage by suppressing c-Fos signaling, suggesting it could be a treatment for age-related macular degeneration.

## Contribution

This study is the first to demonstrate PQQ's protective effects in an in vivo model of AMD through c-Fos signaling suppression.

## Key findings

- PQQ pretreatment reduced ATR-induced cytotoxicity in ARPE-19 cells in a dose-dependent manner.
- Rats treated with 5 mg/kg PQQ showed significantly better retinal function and preserved photoreceptor layers after light exposure.
- PQQ suppressed light-induced c-Fos upregulation in a dose-dependent manner, linking its protective effects to this signaling pathway.

## Abstract

Age-related macular degeneration (AMD) is a progressive retinal disorder characterised by oxidative stress and inflammation. Although pyrroloquinoline quinone (PQQ) has been reported to exert neuroprotective effects, its specific efficacy in in vivo models of AMD pathophysiology has not yet been elucidated. In this study, we evaluated the protective effects of PQQ against all-trans-retinal (ATR)-induced cytotoxicity in ARPE-19 cells and light-induced photoreceptor degeneration in rats. Pretreatment of ARPE-19 cells with PQQ dose-dependently mitigated ATR-induced cytotoxicity. In the in vivo model, rats received a single intraperitoneal injection of PQQ (2 or 5 mg/kg) 1 h prior to 1000-lux light exposure. Retinal function and morphology were evaluated by electroretinography and haematoxylin–eosin staining, respectively. The 5 mg/kg PQQ group retained significantly greater retinal function than the vehicle group at 3 days postexposure and demonstrated significant preservation of the outer nuclear layer at 7 days postexposure, indicating the suppression of photoreceptor cell death. Western blot analysis detected the dose-dependent suppression of light-induced c-Fos upregulation following PQQ treatment. These findings suggest that the protective effect of PQQ against phototoxic damage is associated with the suppression of c-Fos signalling, thus lending support to the further investigation of PQQ as a potential therapeutic agent for AMD.