Dual suppressive effect of p-coumaric acid on pigmentation in B16F10 cells

Hyperpigmentation, frequently triggered by an excessive production of melanin, is a common issue within the realms of dermatology and cosmetology. In addition to regulating tyrosinase activity, the autophagy process plays a role in melanosome turnover, contributing to pigmentation control. p-Coumaric acid (PCA), a dietary phenolic compound with antioxidant and anti-inflammatory properties, was investigated for its dual suppressive effects on melanin production induced by alpha-melanocyte-stimulating hormone (α-MSH) and autophagy inhibitors in B16F10 cells.

PCA (25–100 µg/mL) serves as a potent in vitro inhibitor of tyrosinase activity. In addition, PCA can effectively mitigate the upregulation of tyrosinase gene expression (P < 0.01) and its cellular activities induced by α-MSH. In contrast to early-stage autophagy inhibitors like SBI0206965 (SBI) and spautin-1, treatment with 50 µM of chloroquine (CQ) and 20 nM of bafilomycin A1 (BFA), both of which inhibit the late stages of the autophagic process, results in an increase in melanin content within B16F10 cells, independent of cellular tyrosinase activity. Furthermore, PCA treatment could protect cells against CQ and BFA-induced lysosomal damage, ultimately leading to the promotion of autolysosome formation and the activation of the autophagic process, which results in melanin degradation.

In summary, PCA exhibits dual suppressive effects on melanogenesis via inhibiting tyrosinase activity and melanin accumulation caused by lysosomal dysfunction. These effects offer an enhanced opportunity for the development of a safe and effective anti-melanogenesis agent.