18β-Glycyrrhetinic acid reduces skin damage from UVB exposure by inhibiting the MyD88/MAPK signaling pathway.

Abstract

Excessive exposure to ultraviolet B (UVB) radiation is a primary cause of skin damage, necessitating the development of effective treatment strategies. 18β-Glycyrrhetinic acid (18β-GA), the principal active compound in Glycyrrhiza glabra, is recognized for its anti-inflammatory, oxidative stress-reducing, and anti-aging properties. This study employs an in vivo model using BALB/c mice with depilated dorsal skin exposed to UVB irradiation, alongside an in vitro model where human skin fibroblast (HSF) cells are subjected to UVB-induced photodamage. The objective is to investigate the therapeutic effects of 18β-GA on UVB-induced skin damage, an area that remains underexplored, and to elucidate the underlying molecular mechanisms. The results demonstrate that 18β-GA significantly alleviates photodamage in skin fibroblasts exposed to UVB, thereby counteracting the aging-associated decline in fibroblast proliferation and the excessive production of reactive oxygen species (ROS). Furthermore, knockdown experiments confirm the involvement of MyD88 in mediating the anti-photodamage effects of 18β-GA. Further in vivo investigations corroborated these findings, demonstrating a significant decrease in UVB-induced skin damage, as evidenced by the reduced expression of proteins linked to the MyD88/MAPK signaling pathway. Through extensive in vitro and in vivo analyses, we elucidated the protective effects of 18β-GA and its underlying molecular mechanisms. These results indicate that 18β-GA may serve as a promising therapeutic agent for mitigating skin damage.