Upregulation of Melanogenesis and Tyrosinase Activity: Potential Agents for Vitiligo

Niu, Chao; Aisa, Haji Akber

doi:10.3390/molecules22081303

Cited by 126 publications

(132 citation statements)

References 116 publications

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“…(Figure 5(a)), but melanin content was dose-dependently inhibited by Rb-ME treatment up to 400 μg/ml (Figure 5(b)), indicating that Rb-ME has a function in melanin production but not secretion. It has been reported that tyrosinase is involved in melanin production [34]; therefore, we confirmed whether Rb-ME can modulate tyrosinase activity. Rb-ME did not directly inhibit mushroom tyrosinase activity ( Figure 5(c)) but significantly inhibited α-MSH-induced cellular tyrosinase activity in B16F10 cells ( Figure 5(d)).…”

Section: Evidence-based Complementary and Alternative Medicine Phosphsupporting

confidence: 83%

Photoaging Protective Effects of Ranunculus bulumei Methanol Extract

Hong

Kim

Cho

2020

Evidence-Based Complementary and Alternative Medicine

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Ultraviolet B (UVB) radiation is the main cause of photoaging processes including cellular senescence, skin drying, collagen degradation, melanogenesis, and inflammation. These responses occur because UVB induces a change in expression of aging-related genes through regulation of signal pathways such as that of mitogen-activated protein kinases- (MAPKs-) activator protein 1 (AP-1). Ranunculus bulumei, which is used as an herb in Indonesia, belongs to the Ranunculaceae family, which has been reported to perform various physiological effects including antioxidant and anti-inflammation. However, data on the pharmaceutical and cosmeceutical utility of Ranunculus bulumei have not been reported. Therefore, we evaluated the antiaging efficacy of RB-ME, a methanol extract of Ranunculus bulumei. Rb-ME attenuated MMP9 and COX-2 gene expression but enhanced SIRT1 and type-1 collagen in UVB-irradiated HaCaT cells. Rb-ME regulated these gene expressions through inhibition of p38 phosphorylation and inactivation of AP-1. In addition, mRNA expression of HAS-2 and -3, which are involved in skin hydration, was elevated in Rb-ME-treated HaCaT cells. Rb-ME also inhibited melanogenesis by suppression of tyrosinase, MITF, and TYRP-1 mRNA in B16F10 cells under α-MSH treatment. Taken together, these results indicate that Rb-ME has a protective effect on some UVB-induced skin photoaging events such as inflammation, collagen degradation, cellular senescence, skin drying, and melanin production through inhibition of the p38-AP-1 signal cascade, indicating that Rb-ME can be used as an active ingredient for antiaging cosmetics.

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Section: Evidence-based Complementary and Alternative Medicine Phosphsupporting

confidence: 83%

Photoaging Protective Effects of Ranunculus bulumei Methanol Extract

Hong

Kim

Cho

2020

Evidence-Based Complementary and Alternative Medicine

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“…The lack of melanization signals, a low level of glutathione (GSH) and loss of melanocytes are indications of ageing, and many scientists have focused on studying the specific mechanism of melanogenesis and developing novel therapeutic medications for hair greying and depigmented skin diseases such as vitiligo . Herein, we investigated the effect of nilotinib (AMN) on the induction of skin pigmentation and the mechanism which elicits activating effects on melanogenesis in murine B16F0 cells.…”

Section: Discussionmentioning

confidence: 99%

Nilotinib induction of melanogenesis via reactive oxygen species‐dependent JNK activation in B16F0 mouse melanoma cells

Chang

Huang

Shen

et al. 2018

Experimental Dermatology

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Nilotinib (AMN), a second‐generation tyrosine kinase inhibitor, induces apoptosis in various cancer cells, and our recent study showed that AMN effectively reduced the viability of human ovarian cancer cells via mitochondrion‐dependent apoptosis. The effect of AMN in the melanogenesis of melanoma cells is still unclear. In the present study, we found that the addition of AMN but not imatinib (STI) significantly increased the darkness of B16F0 melanoma cells, and the absorptive value increased with the concentration of AMN. A decrease in the viability of B16F0 cells by AMN was detected in a concentration‐dependent manner, accompanied by increased DNA ladders, hypodiploid cells and cleavage of the caspase‐3 protein. An in vitro tyrosinase (TYR) activity assay showed that increased TYR activity by AMN was detected in a concentration‐dependent manner; however, induction of TYR activity by STI at a concentration of 40 μmol/L was observed. Increased intracellular peroxide by AMN was detected in B16F0 cells, and application of the antioxidant, N‐acetylcysteine (NAC), significantly reduced AMN‐induced peroxide production which also reduced the darkness of B16F0 cells. Additionally, AMN induced c‐Jun N‐terminal kinase (JNK) protein phosphorylation in B16F0 cells, which was inhibited by the addition of NAC. AMN‐induced melanogenesis of B16F0 cells was significantly inhibited by the addition of NAC and the JNK inhibitor, SP600125 (SP). Data of Western blotting showed that increased protein levels of melanogenesis‐related enzymes of tyrosinase‐related protein‐1 (TRP1), TRP2 and TYR were observed in AMN‐treated B16F0 cells which were inhibited by the addition of NAC and SP. Evidence is provided supporting AMN effectively inducing the melanogenesis of B16F0 melanoma cells via reactive oxygen species‐dependent JNK activation.

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“…Tyrosinase related protein 1 (TRP-1) is believed to catalyze the oxidation of DHICA to melanin. Although all the three enzymes, tyrosinase, TRP-1, and TRP-2 are involved in the melanogenesis pathway, tyrosinase is exclusively necessary for melanogenesis [11,[23][24][25][26][27][28][29][30].…”

Section: Tyrosinase and Its Key Role In Melanin Synthesismentioning

confidence: 99%

Natural and Bioinspired Phenolic Compounds as Tyrosinase Inhibitors for the Treatment of Skin Hyperpigmentation: Recent Advances

2019

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One of the most common approaches for control of skin pigmentation involves the inhibition of tyrosinase, a copper-containing enzyme which catalyzes the key steps of melanogenesis. This review focuses on the tyrosinase inhibition properties of a series of natural and synthetic, bioinspired phenolic compounds that have appeared in the literature in the last five years. Both mushroom and human tyrosinase inhibitors have been considered. Among the first class, flavonoids, in particular chalcones, occupy a prominent role as natural inhibitors, followed by hydroxystilbenes (mainly resveratrol derivatives). A series of more complex phenolic compounds from a variety of sources, first of all belonging to the Moraceae family, have also been described as potent tyrosinase inhibitors. As to the synthetic compounds, hydroxycinnamic acids and chalcones again appear as the most exploited scaffolds. Several inhibition mechanisms have been reported for the described inhibitors, pointing to copper chelating and/or hydrophobic moieties as key structural requirements to achieve good inhibition properties. Emerging trends in the search for novel skin depigmenting agents, including the development of assays that could distinguish between inhibitors and potentially toxic substrates of the enzyme as well as of formulations aimed at improving the bioavailability and hence the effectiveness of well-known inhibitors, have also been addressed.

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Upregulation of Melanogenesis and Tyrosinase Activity: Potential Agents for Vitiligo

Cited by 126 publications

References 116 publications

Photoaging Protective Effects of Ranunculus bulumei Methanol Extract

Photoaging Protective Effects of Ranunculus bulumei Methanol Extract

Nilotinib induction of melanogenesis via reactive oxygen species‐dependent JNK activation in B16F0 mouse melanoma cells

Natural and Bioinspired Phenolic Compounds as Tyrosinase Inhibitors for the Treatment of Skin Hyperpigmentation: Recent Advances

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