Sargahydroquinoic Acid Suppresses Hyperpigmentation by cAMP and ERK1/2-Mediated Downregulation of MITF in α-MSH-Stimulated B16F10 Cells

被引:12
作者
Azam, Mohammed Shariful [1 ]
Kim, Jae-Il [1 ]
Choi, Chang Geun [2 ]
Choi, Jinkyung [1 ]
Lee, Bonggi [1 ]
Kim, Hyeung-Rak [1 ]
机构
[1] Pukyong Natl Univ, Dept Food Sci & Nutr, 45 Yongso Ro, Busan 48513, South Korea
[2] Pukyong Natl Univ, Dept Ecol Engn, 45 Yongso Ro, Busan 48513, South Korea
关键词
cAMP; ERK; hyperpigmentation; melanin; MITF; sargahydroquinoic acid; INHIBITS MELANIN SYNTHESIS; SARGASSUM-SERRATIFOLIUM; ETHANOLIC EXTRACT; TRANSCRIPTION FACTOR; SARGAQUINOIC ACID; RICH FRACTION; MELANOGENESIS; PIGMENTATION; ACTIVATION; MELANOCYTES;
D O I
10.3390/foods10102254
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Hyperpigmentation diseases of the skin require topical treatment with depigmenting agents. We investigated the hypopigmented mechanisms of sargahydroquinoic acid (SHQA) in alpha-melanocyte-stimulating hormone (alpha-MSH)-stimulated B16F10 cells. SHQA reduced cellular tyrosinase (TYR) activity and melanin content in a concentration-dependent manner and attenuated the expression of TYR and tyrosinase-related protein 1 (TRP1), along with their transcriptional regulator, microphthalmia-associated transcription factor (MITF). SHQA also suppressed alpha-MSH-induced cellular production of cyclic adenosine monophosphate (cAMP), which inhibited protein kinase A (PKA)-dependent cAMP-responsive element-binding protein (CREB) activation. Docking simulation data showed a potential binding affinity of SHQA to the regulatory subunit RII beta of PKA, which may also adversely affect PKA and CREB activation. Moreover, SHQA activated ERK1/2 signaling in B16F10 cells, stimulating the proteasomal degradation of MITF. These data suggest that SHQA ameliorated hyperpigmentation in alpha-MSH-stimulated B16F10 cells by downregulating MITF via PKA inactivation and ERK1/2 phosphorylation, indicating that SHQA is a potent therapeutic agent against skin hyperpigmentation disorders.
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页数:13
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