Background

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.

Results

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.

Conclusions

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.

中文翻译：

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对香豆酸对 B16F10 细胞色素沉着的双重抑制作用

背景

色素沉着过度通常由黑色素过度产生引起，是皮肤病学和美容学领域的常见问题。除了调节酪氨酸酶活性外，自噬过程还在黑素体周转中发挥作用，有助于色素沉着控制。对香豆酸 (PCA) 是一种具有抗氧化和抗炎特性的膳食酚类化合物，研究人员研究了其对 B16F10 细胞中由 α-黑素细胞刺激激素 (α-MSH) 和自噬抑制剂诱导的黑色素生成的双重抑制作用。

结果

PCA (25–100 µg/mL) 是一种有效的体外酪氨酸酶活性抑制剂。此外，PCA可以有效减轻α-MSH诱导的酪氨酸酶基因表达上调（P  <0.01）及其细胞活性。与 SBI0206965 (SBI) 和 spautin-1 等早期自噬抑制剂相比，用 50 µM 氯喹 (CQ) 和 20 nM 巴弗洛霉素 A1 (BFA) 治疗（两者均抑制自噬过程的后期），结果B16F10 细胞内黑色素含量增加，与细胞酪氨酸酶活性无关。此外，PCA处理可以保护细胞免受CQ和BFA诱导的溶酶体损伤，最终促进自溶酶体形成并激活自噬过程，从而导致黑色素降解。

结论

总之，PCA通过抑制酪氨酸酶活性和溶酶体功能障碍引起的黑色素积累，对黑色素生成具有双重抑制作用。这些作用为开发安全有效的抗黑素生成剂提供了更多机会。