# Polydatin Prevents UVA-Induced Damage in Human Dermal Fibroblasts by Maintaining Mitochondrial Integrity

## TL;DR

Polydatin protects skin cells from UVA damage by reducing oxidative stress and maintaining healthy mitochondria.

## Contribution

This study reveals polydatin's novel protective role in UVA-induced mitochondrial dysfunction and oxidative stress in fibroblasts.

## Key findings

- Polydatin preserves cell viability and reduces ROS levels after UVA exposure.
- Polydatin maintains mitochondrial membrane potential and respiration.
- Polydatin regulates Nrf2 and reduces mitochondrial fission.

## Abstract

UVA radiation induces oxidative stress, mitochondrial dysfunction, and cell death in human dermal fibroblasts, contributing to skin aging and damage. In this study, we investigated the protective effects of polydatin, a natural polyphenol, against UVA-induced cell damage. Our results show that polydatin preserves cell viability and reduces intracellular reactive oxygen species (ROS) levels after UVA exposure. In addition, polydatin maintains mitochondrial integrity by preserving mitochondrial membrane potential and improving mitochondrial respiration. From a molecular perspective, polydatin regulates the expression of Nrf2, a key regulator of the cellular antioxidant response, thereby promoting cellular defense mechanisms. Additionally, polydatin attenuates UVA-induced mitochondrial fission, supporting a balanced mitochondrial dynamic profile. These results suggest that polydatin exerts a protective effect on UVA-irradiated fibroblasts, highlighting its potential for cosmetic and dermatological applications aimed at preventing photoaging and oxidative skin damage.