Apigenin promotes pigmentation independent of the classic MC1R/cAMP/PKA-pigmentation pathway in HEMCs. (A) HEMCs were treated with apigenin (10 μM) for the indicated time periods (0–180 min), and the phosphorylation of PKA and CREB was assessed by Western blotting. (B) HEMCs were pretreated with or without 10 μM DDA (an AC inhibitor) for 1 h before the addition of apigenin for 48 h. Melanin content, as well as the expression levels of Tyrosinase, MITF, Cdc42, and Rab27a, were measured as described previously. (C) HEMCs were pretreated with or without 10 μM N-1A (an MC1R inhibitor) for 1 h before apigenin treatment for 48 h. Melanin content and the expression levels of Tyrosinase, Cdc42, and Rab27a were measured as described previously. Data are expressed as the mean ± SEM (n = 3). *p < 0.05 vs. untreated cells. MC1R, melanocortin-1 receptor; cAMP, Cyclic Adenosine Monophosphate; PKA, protein kinase A; HEMCs, human epidermal melanocytes; CREB, cAMP response element-binding protein; AC, adenylate cyclase; MITF, Melanocytes inducing transcription factor; Cdc42, cell division cycle 42; Rab27a, Ras-related protein Rab-27a.
|
