Poly‐ <scp>l</scp> ‐Lactic Acid Alleviates <scp>UVB</scp> ‐Induced Photoaging of Dermal Fibroblast (Hs68) and Promotes Collagen Production Through the <scp>MAPK</scp> / <scp>AP</scp> ‐1 Pathway

Photoaging is a skin damage process resulting from prolonged ultraviolet (UV) exposure. Poly-l-lactic acid (PLLA), as a common injectable filler in skin esthetics and anti-aging, is reported to be capable of promoting the synthesis of collagen. However, the potential mechanism remains unclear. This study focused on clarifying the potential molecular mechanisms by which PLLA promotes collagen synthesis in UV-induced skin photoaging. Hs68 cells exposed to UVB (30 mJ/cm²) were employed to simulate skin photoaging. PLLA at different concentrations (100-800 μg/mL) was used to treat cells. The expression of c-Jun, c-Fos, ERK, JNK, and p38 mitogen-activated protein kinase (MAPK) was accomplished by the qPCR. The ROS level and the activities of MMP-1 and MMP-13 were assessed by corresponding kits. The AP-1 activity was evaluated by the dual-luciferase reporter system. Inhibition of MAPK was accomplished by transfection of specific inhibitors. PLLA significantly enhanced the cell viability and reduced ROS production in UVB-exposed Hs68 cells. PLLA contributed a lot to counteracting MMPs activation and collagen degradation induced by UVB exposure. Inhibiting the MAPK pathway not only reduced AP-1 activity but also weakened the activities of MMP-1 and MMP-13. Additionally, the pronounced decline in cell viability and collagen production, as well as the excessive ROS and cell damage, could be ameliorated by inhibiting MAPKs. PLLA significantly alleviated the photoaging of Hs68 cells induced by UVB and effectively promoted the production of collagen via the MAPK/AP-1 pathway.