a-Arbutin Prevents UVA-Induced Skin Photodamage via Alleviating DNA Damage and Collagen Degradation in NIH-3T3 cells
Ultraviolet radiation (UV) causes certain side effects to the skin, and their accumulation to a certain extent can lead to accelerated aging of the skin. Recent studies suggests that a-arbutin may be useful in various disorders such as hyperpigmentation disorders, wound healing, and antioxidant activity. However, the role of a-arbutin in skin photodamage is unclear. In this study, under UVA-induced photodamage conditions, a-arbutin treated mouse skin fibroblasts (NIH-3T3) can repair DNA damage and resist apoptosis by reducing the production of reactive oxygen species (ROS) and increasing the phosphorylation of glycogen synthase kinase 3 beta (GSK3ß) to orchestra AKT/GSK3ß pathway. Meanwhile, a-arbutin can also regulate collagen metabolism and facilitate the replenishment of collagen by targeting the phosphorylation of SMAD3 to mediate the TGFß/SMAD pathway in NIH-3T3. In conclusion, we found that a-arbutin can mitigate the detrimental effects of skin photodamage induced by UVA irradiation, and provides a theoretical basis for the use of a-arbutin in the treatment of skin photodamage. Overall design: After UVA irradiation with the addition of a-arbutin, we wanted to investigate whether a-arbutin had the ability of anti-photodamage in NIH 3T3 cell, especially in DNA repair and collagen synthesis. Then we performed gene expression profiling analysis using data obtained from RNA seq of 3 different treated ways (control group, UVA treated group, UVA and a-arbutin co-treated group)in NIH 3T3 cell.