Anti-pigmentary activity of fucoxanthin and its influence on skin mRNA expression of melanogenic molecules.
OBJECTIVE
Carotenoids and retinoic acid derivatives are topically applied for sun-protective and whitening purposes. Fucoxanthin is a carotenoid derived from edible sea algae, but its effect on melanogenesis has not been established. Therefore, we examined the effect of fucoxanthin on melanogenesis.


METHODS
Inhibitory effects on tyrosinase activity, melanin formation in B16 melanoma and skin pigmentation in UVB-irradiated guinea-pigs were evaluated. To elucidate the action of fucoxanthin on melanogenesis, its effect on skin melanogenic mRNA expression was evaluated in UVB-irradiated mice. Fucoxanthin was given topically or orally to mice once a day and UVB irradiation was applied for 14 days. The effect of fucoxanthin on skin melanogenic mRNA expression was evaluated by real time reverse transcription polymerase chain reaction.


RESULTS
Fucoxanthin inhibited tyrosinase activity, melanogenesis in melanoma and UVB-induced skin pigmentation. Topical application of fucoxanthin (1%) significantly suppressed mRNA expression of cyclooxygenase (COX)-2, endothelin receptor A, p75 neurotrophin receptor (NTR), prostaglandin E receptor 1 (EP1), melanocortin 1 receptor (MC1R) and tyrosinase-related protein 1. The suppression of p75NTR, EP1 and MC1R expressions was observed at 0.01% application. Also, oral application of fucoxanthin (10 mg/kg) significantly suppressed expression of COX-2, p75NTR, EP1 and MC1R.


CONCLUSIONS
These results suggest that fucoxanthin exhibits anti-pigmentary activity by topical or oral application in UVB-induced melanogenesis. This effect of fucoxanthin may be due to suppression of prostaglandin (PG) E(2) synthesis and melanogenic stimulant receptors (neurotrophin, PGE(2) and melanocyte stimulating hormone expression).
Shimoda
Hiroshi
H
Research & Development Division, Oryza Oil & Fat Chemical Co. Ltd, Ichinomiya, Aichi 493-8001, Japan. kaihatsu@mri.biglobe.ne.jp
Tanaka
Junji
J
Shan
Shao-Jie
SJ
Maoka
Takashi
T
D000818:Animals; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology* / Q000627:therapeutic use; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects*; D006168:Guinea Pigs; D008297:Male; D008543:Melanins / Q000037:antagonists & inhibitors* / Q000235:genetics; D008545:Melanoma / Q000517:prevention & control; D051379:Mice; D008812:Mice, Hairless; D014442:Monophenol Monooxygenase / Q000235:genetics / Q000378:metabolism; D000459:Phaeophyceae / Q000737:chemistry*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism; D044102:Receptor, Melanocortin, Type 1 / Q000235:genetics / Q000378:metabolism; D020800:Receptor, Nerve Growth Factor / Q000235:genetics / Q000378:metabolism; D017466:Receptors, Endothelin / Q000235:genetics / Q000378:metabolism; D058306:Receptors, Prostaglandin E, EP1 Subtype / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects; D012880:Skin Pigmentation / Q000187:drug effects* / Q000528:radiation effects; D014466:Ultraviolet Rays; D024341:Xanthophylls / Q000494:pharmacology* / Q000627:therapeutic use
D000972:Antineoplastic Agents, Phytogenic; D008543:Melanins; D010936:Plant Extracts; D012333:RNA, Messenger; D044102:Receptor, Melanocortin, Type 1; D020800:Receptor, Nerve Growth Factor; D017466:Receptors, Endothelin; D058306:Receptors, Prostaglandin E, EP1 Subtype; D024341:Xanthophylls; C025164:fucoxanthin; D014442:Monophenol Monooxygenase; D051546:Cyclooxygenase 2