Melanin homeostasis plays an important role in kaempferide-induced melanogenesis

OBJECTIVE Pathological disorders may lead to abnormal melanin metabolism, such as hyperpigmentation and vitiligo, breaked up the dynamic equilibrium of Melanin Homeostasis. Present work aims to investigate the role of melanin homeostasis of two pigment models response to a melanogenesis inducer, Kaempferide.METHODS The larval zebrafish and primary C57 BL/6 mice epidermis melanocytes were employed used as the nascent pigment model. Adult zebrafish depigmentation model and mice melanoma B16 F10 cell was used as the regenerative pigment models. Morphological changes and melanin content were used to identify the differences of melanin accumulation in both nascent and regenerative pigment models. Transcriptome differential gene analysis and biochemical validation were used to explore the molecular mechanism involved into melanin accumulation and decomposition. RESULTS The accumulation of melanin was observed in both nascent and regenerative pigment models treated with Kaempferide. Remarkably, the nascent pigment model is more sensitive to Kaempferide-induced melanogenesis than regenerative pigment mode in vivo and in vitro. The accumulation of melanin in both models via MC1 R/ACs/MITF signaling pathway and Metabolic enzymes Catechol O-methyltransferase(COMT). However, Entacapone, an inhibitor of COMT, increased melanin accumulation in pigmentation models more than in regenerated pigmentation models.CONCLUSION Melanin homeostasis, involved in melanin metabolism, by promoting melanogenesis and acting on COMT leading to melanogenesis in nascent pigment model,not regenerative pigment model.