Aloperine Attenuates UVB-induced Damage in Skin Fibroblasts Via Activating TFE3/Beclin-1-Mediated Autophagy

Protein Pept Lett. 2024 Nov 15. doi: 10.2174/0109298665335370241017055831. Online ahead of print.

Abstract

Background: Aloperine (ALO) is an important active ingredient in the traditional Chinese medicinal plant Sophora alopecuroides L and has a significant autophagy-stimulating effect. The effect of ALO on cytotoxicity caused by UVB radiation in skin fibroblasts and the potential mechanism remains unclear.

Objective: The present study aimed to assess the effect of ALO on UVB-induced damage in skin fibroblasts and investigate its possible mechanism.

Methods: Cell viability, cytotoxicity, caspase-Glo 3/7 activity, apoptosis, and protein expression were measured in UVB-treated skin fibroblasts in the presence or absence of ALO. Autophagy inhibitors (chloroquine and bafilomycin A1) and TFE3 siRNA transfection were used to elucidate the potential mechanisms further.

Results: These data demonstrate that ALO attenuated cell viability inhibition, apoptosis, cytotoxicity, and alterations in autophagy-related proteins caused by UVB exposure in skin fibroblasts. ALO stimulates autophagy activation and TFE3 nuclear localization in UVB-treated skin fibroblasts. Furthermore, treatment with autophagy inhibitors and TFE3 siRNA reversed the effects of ALO on UVB-treated skin fibroblasts.

Conclusion: These results suggest that ALO protects skin fibroblasts against UVB-induced cytotoxicity by stimulating TFE3/Beclin-1-mediated autophagy.

Keywords: Aloperine; Beclin-1; TFE3; UVB-induced damage; autophagy; skin fibroblasts.