Oleoylethanolamide inhibits α-melanocyte stimulating hormone-stimulated melanogenesis via ERK, Akt and CREB signaling pathways in B16 melanoma cells

Zhou, Juan; Ren, Tong; Liu, Ying; Cheng, Anran; Xie, Wanyi; Xu, Lanxi; Lu, Peng; Lin, Jinbin; Lian, Lianxiang; Diao, Yong; Jin, Xin; Yang, Lichao

doi:10.18632/oncotarget.18097

Cited by 28 publications

(28 citation statements)

References 33 publications

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“…Furthermore, phosphorylation of CREB was significantly suppressed by BHCP. The regulation of α-MSH-induced CREB phosphorylation is known to be potentially important in regulating pigmentation [ 28 ]. These results indicate that the anti-melanogenic effects of BHCP result from the downregulation of MITF and tyrosinase via the downregulation of phosphorylated CREB.…”

Section: Resultsmentioning

confidence: 99%

(2E,5E)-2,5-Bis(3-hydroxy-4-methoxybenzylidene) cyclopentanone Exerts Anti-Melanogenesis and Anti-Wrinkle Activities in B16F10 Melanoma and Hs27 Fibroblast Cells

et al. 2018

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Ultraviolet (UV) radiation exposure is the primary cause of extrinsic skin aging, which results in skin hyperpigmentation and wrinkling. In this study, we investigated the whitening effect of (2E,5E)-2,5-bis(3-hydroxy-4-methoxybenzylidene)cyclopentanone (BHCP) on B16F10 melanoma and its anti-wrinkle activity on Hs27 fibroblasts cells. BHCP was found to potently inhibit tyrosinase, with 50% inhibition concentration (IC50) values of 1.10 µM and 8.18 µM for monophenolase (l-tyrosine) and diphenolase (l-DOPA), and the enzyme kinetics study revealed that BHCP is a competitive-type tyrosinase inhibitor. Furthermore, BHCP significantly inhibited melanin content and cellular tyrosinase activity, and downregulated the levels of microphthalmia-associated transcription factor (MITF), phosphorylated levels of cAMP response element-binding (CREB) protein, and tyrosinase in α-melanocyte stimulating hormone (α-MSH)-induced B16F10 melanoma cells. Moreover, BHCP inhibited the phosphorylation of p65 and expression of matrix metalloproteinases (MMP-1, MMP-9, MMP-12, and MMP-13) in Hs27 fibroblasts stimulated with UV radiation. Therefore, our results demonstrate that BHCP may be a good candidate for the development of therapeutic agents for diseases associated with hyperpigmentation and wrinkling.

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Section: Resultsmentioning

confidence: 99%

(2E,5E)-2,5-Bis(3-hydroxy-4-methoxybenzylidene) cyclopentanone Exerts Anti-Melanogenesis and Anti-Wrinkle Activities in B16F10 Melanoma and Hs27 Fibroblast Cells

et al. 2018

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“…Tyrosinase activity was estimated by measuring the rate of L-DOPA oxidation as previously described, with certain modifications ( 23 ). B16 cells were seeded in a 6-well plate at a density of 3×10 5 cells/well and allowed to attach for 12 h. Then, cells were treated with 1,5-diCQA at 0, 5, 50, 100 µ M or 8-MOP at 50 µ M for 24 h; SB203580 (10 µ M); PD98059 (1 µ M); or SP600125 (10 µ M) for 2 h prior to 1,5-diCQA application.…”

Section: Methodsmentioning

confidence: 99%

Potential anti-vitiligo properties of cynarine extracted from Vernonia anthelmintica (L.) Willd

Mamat

Kabas

et al. 2018

Int J Mol Med

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Vitiligo is a depigmentation disorder of the skin. It is primarily caused by the destruction of melanocytes or obstruction of the melanin synthesis pathway. Melanin is a type of skin pigment that determines skin color. The seeds of Vernonia anthelmintica (L.) Willd (Kaliziri) are used for treating skin diseases including vitiligo in traditional Uyghur medicine. 1,5-Dicaffeoylquinic acid (1,5-diCQA) is a natural polyphenolic compound widely distributed in plants and extracted from Kaliziri seeds. Therefore, in the present study, the effect of 1,5-diCQA on melanin synthesis in B16 cell was evaluated, and its molecular mechanism was explored. The results indicated that 1,5-diCQA treatment of B16 cells stimulated an increase of intracellular melanin level and tyrosinase (TYR) activity without cytotoxicity. Reverse transcription quantitative polymerase chain reaction results also indicated that 1,5-diCQA may markedly improve the protein expression and RNA transcription of microphthalmia-associated transcription factor (MITF), melanogenic enzyme Tyr, tyrosinase-related protein 1 (TRP 1) and tyrosinase-related protein 2 (TRP 2). Additional results identified that 1,5-diCQA may promote the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated kinase (ERK) MAPK. Notably, the increased levels of intracellular melanin synthesis and tyrosinase expression induced by 1,5-diCQA treatment were significantly attenuated by the protein kinase A (PKA) inhibitor H-89. Intracellular cyclic adenosine monophosphate (cAMP) concentration and phosphorylation of cAMP-response element binding protein was increased following 1,5-diCQA treatment. These results indicated that 1,5-diCQA stimulated melanogenesis via the MAPK and cAMP/PKA signaling pathways in B16 cells, which has potential therapeutic implications for vitiligo.

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“…In accordance with these results, SP600125‐induced tyrosinase activity, and the pigmentation of cell pellets was also reduced by kazinol U (Figure D, E). It has been reported that ERK and p38 participate in melanogenesis via MITF and tyrosinase regulation (Bellei et al ., ; Baek and Lee, ; Zhou et al ., ). We found that kazinol U significantly increased p38 and ERK phosphorylation in B16F10 and SK‐MEL‐28 cells (Supporting Information Figure S6B,C).…”

Section: Resultsmentioning

confidence: 97%

Kazinol U inhibits melanogenesis through the inhibition of tyrosinase‐related proteins via AMP kinase activation

Lim

Nam

Jeong

et al. 2019

British J Pharmacology

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Background and Purpose Kazinol U is a prenylated flavan isolated from an extract of Broussonetia kazinoki Sieb (Moraceae). Kazinol U has shown cytoprotective effects against cytokine‐induced apoptotic cell death and induces AMP kinase (AMPK) activation through LKB1 activation. However, kazinol U has not been tested as a regulator of melanogenesis, although bark extract of B. kazinoki has been used as a cosmetic ingredient for skin conditioning. Experimental Approach We cultured mouse, human melanoma cells and normal human melanocytes to demonstrate anti‐melanogenic effects of kazinol U. A tyrosinase activity assay, Western blot, RT‐qPCR and a luciferase reporter gene assay were performed to determine the anti‐melanogenic mechanisms of kazinol U. We confirmed its effect on melanogenesis in vivo using zebrafish. Key Results Kazinol U inhibited the expression and activity of tyrosinase, the rate‐limiting enzyme in melanogenesis, and reduced tyrosinase expression and activity in response to cAMP‐inducing agents. Kazinol U reduced the expression of other melanogenic enzymes, such as tyrosinase‐related protein (Tyrp) 1 and Tyrp2, and down‐regulated microphthalmia‐associated transcription factor (MITF), the master regulator of the tyrosinase gene family. Moreover, kazinol U induced phosphorylation of AMPK and MAPK proteins, which are MITF inhibitors. It also exhibited anti‐melanogenic effects in zebrafish, a recently developed in vivo model. Conclusions and Implications Our findings suggest that kazinol U reduces melanogenesis via its inhibitory effect on MITF and its downstream target genes, tyrosinase, Tyrp1 and Tyrp2. This work may provide a basis for the application of kazinol U for the treatment of hyperpigmentation skin disorders.

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Oleoylethanolamide inhibits α-melanocyte stimulating hormone-stimulated melanogenesis via ERK, Akt and CREB signaling pathways in B16 melanoma cells

Cited by 28 publications

References 33 publications

(2E,5E)-2,5-Bis(3-hydroxy-4-methoxybenzylidene) cyclopentanone Exerts Anti-Melanogenesis and Anti-Wrinkle Activities in B16F10 Melanoma and Hs27 Fibroblast Cells

(2E,5E)-2,5-Bis(3-hydroxy-4-methoxybenzylidene) cyclopentanone Exerts Anti-Melanogenesis and Anti-Wrinkle Activities in B16F10 Melanoma and Hs27 Fibroblast Cells

Potential anti-vitiligo properties of cynarine extracted from Vernonia anthelmintica (L.) Willd

Kazinol U inhibits melanogenesis through the inhibition of tyrosinase‐related proteins via AMP kinase activation

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