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Diosgenin inhibits melanogenesis through the activation of phosphatidylinositol-3-kinase pathway (PI3K) signaling

An increased level of melanin is characteristic of a large number of skin diseases, including acquired hyperpigmentation conditions such as melasma, postinflammatory melanoderma, and solar lentigo. Thus, there is an increasing need for the development of depigmenting agents. In order to evaluate the...

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Published in:Life sciences (1973) 2007-06, Vol.81 (3), p.249-254
Main Authors: Lee, Jongsung, Jung, Kwangseon, Kim, Yeong Shik, Park, Deokhoon
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container_title Life sciences (1973)
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creator Lee, Jongsung
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description An increased level of melanin is characteristic of a large number of skin diseases, including acquired hyperpigmentation conditions such as melasma, postinflammatory melanoderma, and solar lentigo. Thus, there is an increasing need for the development of depigmenting agents. In order to evaluate the depigmenting capacity of diosgenin and elucidate its mechanism of action, several experiments were performed in B16 melanoma cells. Melanin content and Western blots for proteins that are involved in melanogenesis were assessed in this study. The melanin content was significantly inhibited by diosgenin. To clarify the mechanism of the depigmenting property of diosgenin, we examined the involvement of diosgenin in the phosphatidylinositol-3-kinase (PI3K) pathway. In this study, diosgenin inhibited the reduction of Akt and GSK 3β phosphorylation induced by LY294002, a PI3K inhibitor. In accordance with this result, production levels of MITF (microphthalmia-associated transcription factor) and tyrosinase were increased by diosgenin. These data suggest that diosgenin inhibits melanogenesis through the activation of the PI3K pathway. This suggestion was further confirmed by the fact that the increased production level of melanin by LY294002 was reduced by diosgenin in B16 melanoma cells. Our study shows that diosgenin inhibits melanogenesis by activating the PI3K pathway, and also suggests that diosgenin may be an effective inhibitor of hyperpigmentation.
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inhibitors</subject><subject>Monophenol Monooxygenase - biosynthesis</subject><subject>Morpholines - pharmacology</subject><subject>Oncogene Protein v-akt - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - antagonists &amp; inhibitors</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K</subject><subject>Signal Transduction - drug effects</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNp9kE1vEzEQhi0EomnhB3BBPiF62GXs9cdGnFD5qqgEBzhbjtfOTtjY27VTlH-Pq0Tixmk0o-d9pXkIecWgZcDUu107hdxyAN2CbAHWT8iK9XrdgOrYU7IC4KLpOMgLcpnzDgCk1N1zcsG0VL3isCL3HzHlrY8YKcYRN1gy3fvJxlSPPmOmZVzSYTvW6al1BR9swRRpCnQeU57Hug7HCWPKWNLUdM1vjDZ7Otsy_rFH-vbHbfftmmbcRlux7QvyLNgp-5fneUV-ff708-Zrc_f9y-3Nh7vGdZKVJshhLXTgTqyDVaJXQgbbKxs2XGsvmArCOtX3jPMguVegnRWboQcQFjQT3RV5c-qdl3R_8LmYPWbnp_qbT4dsNKgqgXcVZCfQLSnnxQczL7i3y9EwMI-ezc5Uz-bRswFpqueaeX0uP2z2fviXOIutwPsT4OuLD-gXkx366PyAi3fFDAn_U_8XAEePhg</recordid><startdate>20070627</startdate><enddate>20070627</enddate><creator>Lee, Jongsung</creator><creator>Jung, Kwangseon</creator><creator>Kim, Yeong Shik</creator><creator>Park, Deokhoon</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070627</creationdate><title>Diosgenin inhibits melanogenesis through the activation of phosphatidylinositol-3-kinase pathway (PI3K) signaling</title><author>Lee, Jongsung ; 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Thus, there is an increasing need for the development of depigmenting agents. In order to evaluate the depigmenting capacity of diosgenin and elucidate its mechanism of action, several experiments were performed in B16 melanoma cells. Melanin content and Western blots for proteins that are involved in melanogenesis were assessed in this study. The melanin content was significantly inhibited by diosgenin. To clarify the mechanism of the depigmenting property of diosgenin, we examined the involvement of diosgenin in the phosphatidylinositol-3-kinase (PI3K) pathway. In this study, diosgenin inhibited the reduction of Akt and GSK 3β phosphorylation induced by LY294002, a PI3K inhibitor. In accordance with this result, production levels of MITF (microphthalmia-associated transcription factor) and tyrosinase were increased by diosgenin. These data suggest that diosgenin inhibits melanogenesis through the activation of the PI3K pathway. 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subjects Akt
Animals
Blotting, Western
Cell Line, Tumor
Cell Survival - drug effects
Chromones - pharmacology
Diosgenin - pharmacology
Enzyme Inhibitors - pharmacology
Glycogen Synthase Kinase 3 - metabolism
Glycogen Synthase Kinase 3 beta
GSK-3β
Melanin
Melanins - antagonists & inhibitors
Melanins - biosynthesis
Melanoma, Experimental - enzymology
Melanoma, Experimental - metabolism
Mice
Microphthalmia-Associated Transcription Factor - metabolism
MITF
Monophenol Monooxygenase - antagonists & inhibitors
Monophenol Monooxygenase - biosynthesis
Morpholines - pharmacology
Oncogene Protein v-akt - metabolism
Phosphatidylinositol 3-Kinases - antagonists & inhibitors
Phosphatidylinositol 3-Kinases - metabolism
PI3K
Signal Transduction - drug effects
title Diosgenin inhibits melanogenesis through the activation of phosphatidylinositol-3-kinase pathway (PI3K) signaling
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