Document Detail

Rosmarinic acid induces melanogenesis through protein kinase A activation signaling.
MedLine Citation:
PMID:  17651699     Owner:  NLM     Status:  MEDLINE    
Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which play a crucial protective role against skin photocarcinogenesis. In order to determine the effects of rosmarinic acid on melanogenesis and elucidate the molecular events of melanogenesis induced by rosmarinic acid, several experiments were performed in B16 melanoma cells. In this study, we showed that the melanin content and tyrosinase expression were increased by rosmarinic acid in a concentration-dependent manner. In addition, after the melanin content was increased by rosmarinic acid, it was reduced by H-89 and KT 5720, protein kinase A (PKA) inhibitors, but not by SB203580, a p38(mapk) inhibitor, or Ro-32-0432, a PKC inhibitor, which suggests the involvement of PKA in rosmarinic acid-induced melanogenesis. Consistent with this, rosmarinic acid induced the phosphorylation of CRE-binding protein (CREB), but had no effect on the phosphorylation of p38(mapk) or the inhibition of Akt phosphorylation. Additionally, rosmarinic acid induced the activation of cAMP response element (CRE) without having any effect on cAMP production, which suggests that rosmarinic acid-induced melanogenesis is mediated by PKA, which occurs downstream of cAMP production. This result was further confirmed by the fact that rosmarinic acid-induced phosphorylation of CREB was inhibited by H-89, but not by PD98059, a MEK1 inhibitor, or by LY294002, a phosphatidylinositol-3-kinase (PI3K) inhibitor. Rosmarinic acid-induced expression of tyrosinase protein was attenuated by H-89. Based on these results, we report for the first time that rosmarinic acid induces melanogenesis through PKA activation signaling.
Jongsung Lee; Yeong Shik Kim; Deokhoon Park
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-06-14
Journal Detail:
Title:  Biochemical pharmacology     Volume:  74     ISSN:  0006-2952     ISO Abbreviation:  Biochem. Pharmacol.     Publication Date:  2007 Oct 
Date Detail:
Created Date:  2007-08-27     Completed Date:  2007-10-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0101032     Medline TA:  Biochem Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  960-8     Citation Subset:  IM    
Biospectrum Life Science Institute, SK Ventium 101-701, Dangjung Dong, Gunpo City, 436-776 Kyunggi-do, Republic of Korea.
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MeSH Terms
Carbazoles / pharmacology
Cell Line, Tumor
Cinnamates / pharmacology*
Cyclic AMP / metabolism
Cyclic AMP Response Element-Binding Protein / metabolism
Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors,  metabolism*
Depsides / pharmacology*
Enzyme Activation
Indoles / pharmacology
Isoquinolines / pharmacology
Melanins / biosynthesis*
Melanoma / drug therapy,  metabolism*
Monophenol Monooxygenase / metabolism
Oncogene Protein v-akt / metabolism
Pyrroles / pharmacology
Signal Transduction
Sulfonamides / pharmacology
p38 Mitogen-Activated Protein Kinases
Reg. No./Substance:
0/Carbazoles; 0/Cinnamates; 0/Cyclic AMP Response Element-Binding Protein; 0/Depsides; 0/Indoles; 0/Isoquinolines; 0/Melanins; 0/Pyrroles; 0/Sulfonamides; 108068-98-0/KT 5720; 127243-85-0/H 89; 537-15-5/rosmarinic acid; 60-92-4/Cyclic AMP; EC Monooxygenase; EC Protein v-akt; EC AMP-Dependent Protein Kinases; EC Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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