Aglycone of Rh4 inhibits melanin synthesis in B16 melanoma cells: Possible involvement of the protein kinase A pathway

Yun Mi Jeong; Won Keun Oh; Tien Lam Tran; Wang Kyun Kim; Sang Hyun Sung; Kyeol Bae; Suman Lee; Jong Hyuk Sung

doi:10.1271/bbb.120602

Aglycone of Rh₄ inhibits melanin synthesis in B16 melanoma cells: Possible involvement of the protein kinase A pathway

Yun Mi Jeong, Won Keun Oh, Tien Lam Tran, Wang Kyun Kim, Sang Hyun Sung, Kyeol Bae, Suman Lee, Jong Hyuk Sung

Department of Pharmacy

Research output: Contribution to journal › Article › peer-review

32 Citations (Scopus)

Abstract

To our knowledge, there is no report that directly shows an inhibitory effect of ginsenoside on melanin synthesis in B16 melanoma cells. Hence, we investigated whether the aglycone of Rh₄ (A-Rh₄) inhibits melanin synthesis in B16 melanoma cells, and determined the mechanism of melanin inhibition. We isolated 12 ginsenoside compounds from leaves of Panax ginseng and tested them in B16 melanoma cells. It significantly reduced melanin content and tyrosinase activity under alpha-melanocyte stimulating hormone- and forskolinstimulated conditions. It significantly reduced the cyclic AMP (cAMP) level in B16 melanoma cells, and this might be responsible for the regulation down of MITF and tyrosinase. Phosphorylation of a downstream molecule, a cAMP response-element binding protein, was significantly decreased according to Western blotting and immunofluorescence assay. These data suggest that A-Rh ₄ has an anti-melanogenic effect via the protein kinase A pathway.

Original language	English
Pages (from-to)	119-125
Number of pages	7
Journal	Bioscience, Biotechnology and Biochemistry
Volume	77
Issue number	1
DOIs	https://doi.org/10.1271/bbb.120602
Publication status	Published - 2013

Bibliographical note

Funding Information:
This research was supported by a grant (C10102410) from the Gyeonggi Technology Development Program funded by Gyeonggi Province in Korea. The authors declare that they have no competing financial interests.

All Science Journal Classification (ASJC) codes

Biotechnology
Analytical Chemistry
Biochemistry
Applied Microbiology and Biotechnology
Molecular Biology
Organic Chemistry

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10.1271/bbb.120602

Cite this

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title = "Aglycone of Rh4 inhibits melanin synthesis in B16 melanoma cells: Possible involvement of the protein kinase A pathway",

abstract = "To our knowledge, there is no report that directly shows an inhibitory effect of ginsenoside on melanin synthesis in B16 melanoma cells. Hence, we investigated whether the aglycone of Rh4 (A-Rh4) inhibits melanin synthesis in B16 melanoma cells, and determined the mechanism of melanin inhibition. We isolated 12 ginsenoside compounds from leaves of Panax ginseng and tested them in B16 melanoma cells. It significantly reduced melanin content and tyrosinase activity under alpha-melanocyte stimulating hormone- and forskolinstimulated conditions. It significantly reduced the cyclic AMP (cAMP) level in B16 melanoma cells, and this might be responsible for the regulation down of MITF and tyrosinase. Phosphorylation of a downstream molecule, a cAMP response-element binding protein, was significantly decreased according to Western blotting and immunofluorescence assay. These data suggest that A-Rh 4 has an anti-melanogenic effect via the protein kinase A pathway.",

author = "Jeong, {Yun Mi} and Oh, {Won Keun} and Tran, {Tien Lam} and Kim, {Wang Kyun} and Sung, {Sang Hyun} and Kyeol Bae and Suman Lee and Sung, {Jong Hyuk}",

note = "Funding Information: This research was supported by a grant (C10102410) from the Gyeonggi Technology Development Program funded by Gyeonggi Province in Korea. The authors declare that they have no competing financial interests.",

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T2 - Possible involvement of the protein kinase A pathway

AU - Jeong, Yun Mi

AU - Oh, Won Keun

AU - Tran, Tien Lam

AU - Kim, Wang Kyun

AU - Sung, Sang Hyun

AU - Bae, Kyeol

AU - Lee, Suman

AU - Sung, Jong Hyuk

N1 - Funding Information: This research was supported by a grant (C10102410) from the Gyeonggi Technology Development Program funded by Gyeonggi Province in Korea. The authors declare that they have no competing financial interests.

PY - 2013

Y1 - 2013

N2 - To our knowledge, there is no report that directly shows an inhibitory effect of ginsenoside on melanin synthesis in B16 melanoma cells. Hence, we investigated whether the aglycone of Rh4 (A-Rh4) inhibits melanin synthesis in B16 melanoma cells, and determined the mechanism of melanin inhibition. We isolated 12 ginsenoside compounds from leaves of Panax ginseng and tested them in B16 melanoma cells. It significantly reduced melanin content and tyrosinase activity under alpha-melanocyte stimulating hormone- and forskolinstimulated conditions. It significantly reduced the cyclic AMP (cAMP) level in B16 melanoma cells, and this might be responsible for the regulation down of MITF and tyrosinase. Phosphorylation of a downstream molecule, a cAMP response-element binding protein, was significantly decreased according to Western blotting and immunofluorescence assay. These data suggest that A-Rh 4 has an anti-melanogenic effect via the protein kinase A pathway.

AB - To our knowledge, there is no report that directly shows an inhibitory effect of ginsenoside on melanin synthesis in B16 melanoma cells. Hence, we investigated whether the aglycone of Rh4 (A-Rh4) inhibits melanin synthesis in B16 melanoma cells, and determined the mechanism of melanin inhibition. We isolated 12 ginsenoside compounds from leaves of Panax ginseng and tested them in B16 melanoma cells. It significantly reduced melanin content and tyrosinase activity under alpha-melanocyte stimulating hormone- and forskolinstimulated conditions. It significantly reduced the cyclic AMP (cAMP) level in B16 melanoma cells, and this might be responsible for the regulation down of MITF and tyrosinase. Phosphorylation of a downstream molecule, a cAMP response-element binding protein, was significantly decreased according to Western blotting and immunofluorescence assay. These data suggest that A-Rh 4 has an anti-melanogenic effect via the protein kinase A pathway.

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