• 약학회지
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• 제47권6호
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• pp.404-409
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• 2003

To investigate the effect of chitosan oligosaccharide on melanin synthesis, we measured tyrosinase activity and melanin production in B16 melanoma cells. Chitosan oligosacchaide itself did not have any anti-oxidant activity in DPPH radical scavenging, and did not affect the proliferation of B16 melanoma cells. Chitosan oligosaccharide dose-dependently increased melanin production in the absence or presence of MSH. However, chitosan oligosaccharide did not have any influence on the tyrosinase activity and tyrosinase expression in B16 melanoma cells. These results suggest that chitosan oligosaccharide-induced melanin production may be independent on tyrosinase activity in B16 melanoma cells. From the above results. chitosan oligosaccharide dose-dependently appears to increase melanin production in B16 melanoma cells, suggesting that chitosan oligosaccharide may be used as a tanning agent.

• 동의생리병리학회지
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• 제23권1호
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• pp.63-75
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• 2009

The aim of this study was to elucidate the antimelanogenic effect of Dokhwalkisaeng-tang(Duohujisheng-tang) in B16F10 melanoma cells. Dokhwalkisaeng-tang(DKT) was used to develop the effective prescription of inhibition of melanin production. We determined inhibitory effects of DKT on melanin-release, melanin production, and tyrosinase activity in B16F10 melanoma cells. And to explicate the action-mechanism of DKT, melanin-related gene expressions were determined using RT-PCR and real time RT PCR technique in B16F10 melanoma cells. DKT inhibited melanin-release, melanin production in B16F10 melanoma cells considerably. DKT inhibited tyrosinase activity in vitro and in B16F10 melanoma cells. DKT inhibited the expression of tyrosinase, TRP-1, TRP-2 in B16F10 melanoma cells. DKT inhibited the expression of PKA, PKC, MMP-2 and MITF in B16F10 melanoma cells. On the other hand, DKT increased the expression of ERK-1, ERK-2, AKT-1 in B16F10 melanoma cells. From these results, we propose that DKT may have effect on the antimelanogenesis.

• 대한한방부인과학회지
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• 제22권4호
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• pp.1-18
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Mibaeksan (MB) on melanin synthesis in B16F10 mouse melanoma cell. Methods: To demonstrate the inhibitory effects of MB on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma cell. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma cell. And to investigate the action mechanism, we assessed the gene expression of tyrosinase, TRP-1, TRP-2, MMP-2, PKA, $PKC{\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma cells. Results: 1. MB decreased the release and production of melanin in B16F10 melanoma cells. 2. MB decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. MB decreased the expression of tyrosinase, TRP-1, TRP-2, PKA, $PKC{\beta}$ and MMP-2 in B16F10 melanoma cells. 4. MB increased the expression of ERK-1, ERK-2 and AKT-1 in B16F10 melanoma cells. 5. MB decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, it may be concluded that MB has the antimelanogenetic effects.

• 대한한방부인과학회지
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• 제22권4호
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• pp.28-45
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Yukmijihwangtanghapyijihwangagambang (YM) on melanin synthesis in B16F10 melanoma cells. Methods: To demonstrate the inhibitory effects of YM on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma call. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma call. And to investigate the action mechanism, we assessed the gene expression of tyrosinase, TRP-1, TRP-2, PKA, $PKC{\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma call. Results: 1. YM decreased the release and production of melanin in B16F10 melanoma cells. 2. YM decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. YM decreased the expression of tyrosinase, TRP-1, TRP-2 in B16F10 melanoma cells. 4. YM decreased the expression of PKA, $PKC{\beta}$ in B16F10 melanoma cells. 5. YM increased the expression of ERK-1, ERK-2 and AKT-1 in B16F10 melanoma cells. 6. YM decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, it may be concluded that YM has antimelanogenetic effects.

• 약학회지
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• 제46권1호
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• pp.75-80
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• 2002

Quercetin is one of the bioflavonoid compounds and has multiple biological effects such as antioxidant and effective anti-inflammatory agent. Melanin has an important role in protecting human skin from the damaging effects of ultra-violet W) radiation. We studied the effect of quercetin on proliferation of B16/F10 melanoma cells. After 48h treatment of cells with quercetin, the cells exhibited a dose-dependent inhibition in their proliferation without apoptosis. Therefore, the decrease in cell numbers may be due to cell growth arrest, not due to cell death by cytotoxicity. We also investigated the effect of quercetin on melanogenesis of this cells. B16/F10 melanoma cells were grown for 48h in the presence of 0.01~50$\mu\textrm{g}$/ml quercetin and the total melanin contents were measured. Quercetin stimulated melanization of the cells in low concentrations (0.01~20$\mu\textrm{g}$/ml), whereas it inhibited melanization in high concentrations (30~50$\mu\textrm{g}$/ml). It was observed that quercetin differently regulates melanogenesis of B16/F10 melanoma cells dependent on its concentrations.

• 대한한방부인과학회지
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• 제22권3호
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• pp.66-82
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Yukmijihwangtang-gagambang (YMG) on melanin synthesis in B16F10 mouse melanoma cell. Methods: To demonstrate the inhibitory effects of YMG on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma cell. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma cell. And to investigate the action mechanism we assessed the gene expressions of tyrosinase, TRP-1, TRP-2, MMP-2, PKA, PKC${\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma cells. Results: 1. YMG decreased the release and production of melanin in B16F10 melanoma cells. 2. YMG decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. YMG decreased the expression of tyrosinase, TRP-1, TRP-2, PKA, PKC${\beta}$ and MMP-2 in B16F10 melanoma cells. 4. YMG increased the expression of ERK-1, ERK-2, and AKT-1 in B16F10 melanoma cells. 5. YMG decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, we suggest that YMG inhibit melanin synthesis via tyrosinase inhibition and regulation of the gene expression in B16F10 melanoma cells.

• Toxicological Research
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• 제22권4호
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• pp.349-356
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• 2006

Diallyl disulfide (DADS), an oil-soluble organosulfur compound in garlic has been reported to suppress tumor growth and to induce apoptosis in cancer. In the present study, we investigated the effects of DADS on pulmonary metastasis of B16-F10 murine melanoma cells. DADS (i.p. 40 mg/kg) significantly (p<0.05) reduced the number of pulmonary metastatic nodules (48%) in experimental pulmonary metastasis assay. We also found that DADS inhibited adhesion, invasion and migration of B16-F10 melanoma cells in a dose-dependent manner. To study the antimetastatic potential of DADS, we performed the effects of DADS on matrix metalloproteinase activity. DADS significantly inhibited the expression of matrix metalloproteinase-2 activity in B16-F10 cells by gelatin zymography. These results suggest that DADS prevent metastasis in part through suppression of migration of B16-F10 melanoma cells by Inhibiting matrix metalloproteirase-2 responsible for degradation of extracellar matrix.

• 약학회지
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• 제52권6호
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• pp.500-506
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• 2008

Apigenin, a natural flavonoid found in a variety of vegetables and fruits, has been shown to possess many biological functions. In this study we found that apigenin stimulated melanin synthesis in a dose-dependent manner in B16 murine melanoma cells. Since in our previous study $K^+$-$Cl^-$-cotransport (KCC) has been shown to mediate the mechanism of action of apigenin in neuronal cells, we further investigated the role of KCC in the melanogenesis-stimulating effect of apigenin in B16 cells. At nontoxic concentrations apigenin induced $Cl^-$-dependent $K^+$ efflux, a hallmark of KCC activity, which was markedly prevented by a specific KCC inhibitor R-(+)-[(2-n-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy]acetic acid (DIOA). These results indicate that KCC is functionally present, and activated by apigenin in the B16 cells. In addition, the apigenin-induced stimulation of melanogenesis was also significantly inhibited by DIOA. NEthylmaleimide (NEM), a known KCC activator, induced $Cl^-$ efflux and stimulated melanogenesis in a concentration-dependent fashion. Both effects of NEM were significantly inhibited by DIOA. Taken together, these results suggest that apigenin can modulate melanogenesis through the activation of a membrane ion transporter, KCC in B16 cells. These results further suggest that apigenin may be a good candidate in the therapeutic strategy for hypopigmentation disorders, such as vitiligo.

• 약학회지
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• 제55권6호
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• pp.485-491
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• 2011

Previously, we have reported that apigenin, a natural flavonoid found in a variety of vegetables and fruits, stimulated melanogenesis through the activation of $K^+-Cl^-$-cotransport (KCC) in B16 melanoma cells. In this study we investigated the possible involvement of reactive oxygen species (ROS) in the mechanism of apigenin-induced melanogenesis in B16 cells. Apigenin elevated intracellular ROS level in a dose-dependent manner. Treatment with various inhibitors of NADPH oxidase, diphenylene iodonium (DPI), apocynin (Apo) and neopterine (NP) significantly inhibited both the generation of ROS and melanogenesis induced by apigenin. In addition these inhibitors profoundly inhibited apigenin-induced $Cl^-$-dependent $K^+$ efflux, a hallmark of KCC activity. However, the apigenin-induced ROS generation was not significantly affected by treatment with a specific KCC inhibitor R-(+)-[(2-n-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy]acetic acid (DIOA). These results indicate that the ROS production may be a upstream regulator of the apigenin-induced KCC stimulation, and in turn, melanogenesis in the B16 cells. Taken together, these results suggest that the NADPH oxidase-mediated ROS production may play an important role in the apigenin-induced melanogenesis in B16 cells. These results further suggest that NADPH oxidase may be a good target for the management of hyperpigmentation disorders.

• Journal of Applied Biological Chemistry
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• 제64권4호
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• pp.447-451
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• 2021

In this study, we discovered for the first time that linarin, a flavonoid compound, enhances melanin biosynthesis in B16F10 cells, and subsequently elucidated the underlying mechanism of linarin-induced melanogenesis. Linarin showed no cytotoxicity at a concentration of 42 μM and significantly increased intracellular tyrosinase activity and melanin content in B16F10 cells. Mechanistic analysis showed that linarin increased the expression of tyrosinase, tyrosinase-related protein 1 (TRP-1), and microphthalmia-associated transcription factor (MITF) that are related to melanogenesis. Moreover, linarin decreased the phosphorylation of extracellular signal-regulated kinase (ERK) and protein kinase B (AKT). Finally, we evaluated the effect of the structure-activity relationship of linarin and its aglycone on melanogenesis. The results indicated that linarin enhances the expression of melanogenic proteins by activating MITF expression via the modulation of mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K), and protein kinase B signaling pathways in B16F10 cells, thereby enhancing melanogenesis.