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Anti-melanogenic effects of oyster hydrolysate in UVB-irradiated C57BL/6J mice and B16F10 melanoma cells via downregulation of cAMP signaling pathway.
Journal of Ethnopharmacology 2019 January 31
ETHNOPHARMACOLOGICAL RELEVANCE: Pacific oyster (Crassostrea gigas) has been used to treat pigmentary disorders such as freckles, melasma, and moles in Korea.
AIM OF THE STUDY: We aimed to investigate the inhibitory effects of oyster hydrolysate (OH) on melanogenesis in B16F10 melanoma cells and UVB-irradiated C57BL/6J mice.
MATERIAL AND METHODS: The molecular weight distribution and peptide sequences of OH were detected using MALDI-TOF and UHPLC. To evaluate the anti-melanogenic effects of OH, cell viability, melanin content, tyrosinase activity, intracellular cyclic adenosine monophosphate (cAMP) and protein expressions levels were measured in B16F10 cells. In addition, OH was orally administered to UVB-irradiated mice for 9 weeks. After sacrificing the mice, the whitening effects of OH were evaluated based on histological observations and protein expression levels.
RESULTS: In B16F10 cells, OH decreased melanin content and tyrosinase activity in a dose-dependent manner. OH exhibited anti-melanogenic activities via downregulation of cAMP signaling pathway, which consequently decreased melanin synthesis. In UVB-irradiated mice groups, OH decreased the number of active melanocytes and melanin granules. The expression of tyrosinase-related proteins and microphthalmia-associated transcription factor (MITF) decreased in the OH-administered groups.
CONCLUSIONS: These results show that OH inhibits melanin synthesis in B16F10 cells via downregulation of cAMP signaling pathway and in UVB-irradiated mice, by decreasing the number of active melanocytes and melanin granules.
AIM OF THE STUDY: We aimed to investigate the inhibitory effects of oyster hydrolysate (OH) on melanogenesis in B16F10 melanoma cells and UVB-irradiated C57BL/6J mice.
MATERIAL AND METHODS: The molecular weight distribution and peptide sequences of OH were detected using MALDI-TOF and UHPLC. To evaluate the anti-melanogenic effects of OH, cell viability, melanin content, tyrosinase activity, intracellular cyclic adenosine monophosphate (cAMP) and protein expressions levels were measured in B16F10 cells. In addition, OH was orally administered to UVB-irradiated mice for 9 weeks. After sacrificing the mice, the whitening effects of OH were evaluated based on histological observations and protein expression levels.
RESULTS: In B16F10 cells, OH decreased melanin content and tyrosinase activity in a dose-dependent manner. OH exhibited anti-melanogenic activities via downregulation of cAMP signaling pathway, which consequently decreased melanin synthesis. In UVB-irradiated mice groups, OH decreased the number of active melanocytes and melanin granules. The expression of tyrosinase-related proteins and microphthalmia-associated transcription factor (MITF) decreased in the OH-administered groups.
CONCLUSIONS: These results show that OH inhibits melanin synthesis in B16F10 cells via downregulation of cAMP signaling pathway and in UVB-irradiated mice, by decreasing the number of active melanocytes and melanin granules.
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