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Hesperidin, A Popular Antioxidant Inhibits Melanogenesis via Erk1/2 Mediated MITF Degradation.

Lee HJ, Lee WJ, Chang SE, Lee GY - Int J Mol Sci (2015)

Bottom Line: In results, hesperidin strongly inhibited melanin synthesis and tyrosinase activity.Hesperidin decreased tyrosinase, TRP-1, and TRP-2 protein expression but increased phospho-extracellular signal-regulated kinase 1/2 (p-Erk1/2) expression.Taken together, hesperidin, a popular antioxidant, stimulated Erk1/2 phosphorylation which subsequently degraded MITF which resulted in suppression of melanogenic enzymes and melanin synthesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Pyeong-dong, Jongno-gu, Seoul 110-746, Korea. heunjoolee111@gmail.com.

ABSTRACT
Regulation of melanogenesis has been the focus of treatment for hyperpigmentary skin disorders. Although hesperidin is one of the most well-known, naturally occurring flavonoids with antioxidant and anti-inflammatory effect, its anti-melanogenic effect is not known. The present study aims to determine the anti-melanogenic effect of hespiridin as well as its underlying molecular mechanisms. Melanin contents were measured in normal human melanocytes and B16F10 melanoma cells. Protein and mRNA levels of tyrosinase, microphthalmia-associated transcription factor (MITF), tyrosinase related protein-1 (TRP-1) and TRP-2 were determined. Melanogenesis-regulating signals were examined. In results, hesperidin strongly inhibited melanin synthesis and tyrosinase activity. Hesperidin decreased tyrosinase, TRP-1, and TRP-2 protein expression but increased phospho-extracellular signal-regulated kinase 1/2 (p-Erk1/2) expression. Specific inhibitor of Erk1/2 or proteasome inhibitor reversed the inhibition of melanogenesis induced by hesperidin. Taken together, hesperidin, a popular antioxidant, stimulated Erk1/2 phosphorylation which subsequently degraded MITF which resulted in suppression of melanogenic enzymes and melanin synthesis.

No MeSH data available.


Related in: MedlinePlus

Effect of co-treatment with hesperidin and MG132 (protease inhibitor) on (a) melanin contents and (b) MITF protein expressions in B16F10 cells. Cells were incubated with MG132 with or without hesperidin. Melanogenesis-related protein expressions were analyzed by Western blot. Each percentage value for the treated cells was reported relative to that in α-MSH-stimulated cells. Data were expressed as mean ± SD of three independent experiments carried out in triplicates. ** p < 0.01 as compared to the one treated with hesperidin (30 μM) only.
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ijms-16-18384-f005: Effect of co-treatment with hesperidin and MG132 (protease inhibitor) on (a) melanin contents and (b) MITF protein expressions in B16F10 cells. Cells were incubated with MG132 with or without hesperidin. Melanogenesis-related protein expressions were analyzed by Western blot. Each percentage value for the treated cells was reported relative to that in α-MSH-stimulated cells. Data were expressed as mean ± SD of three independent experiments carried out in triplicates. ** p < 0.01 as compared to the one treated with hesperidin (30 μM) only.

Mentions: Then, we examined whether the hesperidin-mediated decrease in MITF protein levels results from its proteasome-dependent degradation of MITF protein. B16F10 cells were incubated with hesperidin for 72 h in the absence or presence of the proteasome-specific inhibitor MG132. Intriguingly, MG132 reversed the suppression of melanin synthesis by hesperidin (Figure 5a) and also prevented the hesperidin-mediated decrease in levels of MITF protein (Figure 5b).


Hesperidin, A Popular Antioxidant Inhibits Melanogenesis via Erk1/2 Mediated MITF Degradation.

Lee HJ, Lee WJ, Chang SE, Lee GY - Int J Mol Sci (2015)

Effect of co-treatment with hesperidin and MG132 (protease inhibitor) on (a) melanin contents and (b) MITF protein expressions in B16F10 cells. Cells were incubated with MG132 with or without hesperidin. Melanogenesis-related protein expressions were analyzed by Western blot. Each percentage value for the treated cells was reported relative to that in α-MSH-stimulated cells. Data were expressed as mean ± SD of three independent experiments carried out in triplicates. ** p < 0.01 as compared to the one treated with hesperidin (30 μM) only.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581251&req=5

ijms-16-18384-f005: Effect of co-treatment with hesperidin and MG132 (protease inhibitor) on (a) melanin contents and (b) MITF protein expressions in B16F10 cells. Cells were incubated with MG132 with or without hesperidin. Melanogenesis-related protein expressions were analyzed by Western blot. Each percentage value for the treated cells was reported relative to that in α-MSH-stimulated cells. Data were expressed as mean ± SD of three independent experiments carried out in triplicates. ** p < 0.01 as compared to the one treated with hesperidin (30 μM) only.
Mentions: Then, we examined whether the hesperidin-mediated decrease in MITF protein levels results from its proteasome-dependent degradation of MITF protein. B16F10 cells were incubated with hesperidin for 72 h in the absence or presence of the proteasome-specific inhibitor MG132. Intriguingly, MG132 reversed the suppression of melanin synthesis by hesperidin (Figure 5a) and also prevented the hesperidin-mediated decrease in levels of MITF protein (Figure 5b).

Bottom Line: In results, hesperidin strongly inhibited melanin synthesis and tyrosinase activity.Hesperidin decreased tyrosinase, TRP-1, and TRP-2 protein expression but increased phospho-extracellular signal-regulated kinase 1/2 (p-Erk1/2) expression.Taken together, hesperidin, a popular antioxidant, stimulated Erk1/2 phosphorylation which subsequently degraded MITF which resulted in suppression of melanogenic enzymes and melanin synthesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Pyeong-dong, Jongno-gu, Seoul 110-746, Korea. heunjoolee111@gmail.com.

ABSTRACT
Regulation of melanogenesis has been the focus of treatment for hyperpigmentary skin disorders. Although hesperidin is one of the most well-known, naturally occurring flavonoids with antioxidant and anti-inflammatory effect, its anti-melanogenic effect is not known. The present study aims to determine the anti-melanogenic effect of hespiridin as well as its underlying molecular mechanisms. Melanin contents were measured in normal human melanocytes and B16F10 melanoma cells. Protein and mRNA levels of tyrosinase, microphthalmia-associated transcription factor (MITF), tyrosinase related protein-1 (TRP-1) and TRP-2 were determined. Melanogenesis-regulating signals were examined. In results, hesperidin strongly inhibited melanin synthesis and tyrosinase activity. Hesperidin decreased tyrosinase, TRP-1, and TRP-2 protein expression but increased phospho-extracellular signal-regulated kinase 1/2 (p-Erk1/2) expression. Specific inhibitor of Erk1/2 or proteasome inhibitor reversed the inhibition of melanogenesis induced by hesperidin. Taken together, hesperidin, a popular antioxidant, stimulated Erk1/2 phosphorylation which subsequently degraded MITF which resulted in suppression of melanogenic enzymes and melanin synthesis.

No MeSH data available.


Related in: MedlinePlus