Hydrolyzed cow colostrum extract (BCFM) inhibits alpha-MSH-induced melanogenesis in B16F1 cells via regulation of the MC1R-cAMP signaling pathway

Cow colostrum is the first milk produced after birth and is a rich natural source of nutrients, immunoglobulins, peptides, and growth factors. The bioconversion of milk and whey changes the immobilization and biochemical characterization. However, the cellular mechanism and the anti-melanin synthesis effects of hydrolyzed cow colostrum extract (BCFM) in alpha-MSH-induced B16F1 cells have not been examined. In this study, we investigated the anti-melanogenesis mechanism by examining the effects of BCFM in alpha-MSH-induced B16F1 cells. Cells were treated with BCFM in the presence or absence of alpha-MSH and co-cultured for 24, 48, and 72 h. The treatment of B16F1 cells with alpha-MSH resulted in the darkening of the color of the cells and induction of melanin synthesis. In addition, the expression levels of MC1R and cAMP, as well as phosphorylation levels of CREB and PKA, were increased by alpha-MSH treatment. However, concomitant treatment with BCFM resulted in a significant decrease in these factors and phosphorylated MITF. At the same time, the expressive amount of TRP-1 and tyrosinase was also decreased in B16F1 cells. These results demonstrate the potential of BCFM for the prevention of melanogenesis progression via the regulation of the MC1R-cAMP signaling pathway in alpha-MSH-induced B16F1 cells. The administration of BCFM suppressed the expression of TRP-1 and/or tyrosinase by regulating the CREB/MITF signaling pathways in the B16F1 cells. We propose that hydrolyzed cow colostrum extract (BCFM) is suitable for use as a novel active agent for skin whitening or pharmaceutical applications.