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Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells

BACKGROUND: Ginsenoside Rf is a ginseng saponin found only in Panax ginseng that affects lipid metabolism. It also has neuroprotective and antiinflammatory properties. We previously showed that Korean Red Ginseng (KRG) inhibited the expression of cyclooxygenase-2 (COX-2) by hypoxia via peroxisome pr...

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Autores principales: Song, Heewon, Park, Joonwoo, Choi, KeunOh, Lee, Jeonggeun, Chen, Jie, Park, Hyun-Ju, Yu, Byeung-Il, Iida, Mitsuru, Rhyu, Mee-Ra, Lee, YoungJoo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6437553/
https://www.ncbi.nlm.nih.gov/pubmed/30976170
http://dx.doi.org/10.1016/j.jgr.2018.11.007
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author Song, Heewon
Park, Joonwoo
Choi, KeunOh
Lee, Jeonggeun
Chen, Jie
Park, Hyun-Ju
Yu, Byeung-Il
Iida, Mitsuru
Rhyu, Mee-Ra
Lee, YoungJoo
author_facet Song, Heewon
Park, Joonwoo
Choi, KeunOh
Lee, Jeonggeun
Chen, Jie
Park, Hyun-Ju
Yu, Byeung-Il
Iida, Mitsuru
Rhyu, Mee-Ra
Lee, YoungJoo
author_sort Song, Heewon
collection PubMed
description BACKGROUND: Ginsenoside Rf is a ginseng saponin found only in Panax ginseng that affects lipid metabolism. It also has neuroprotective and antiinflammatory properties. We previously showed that Korean Red Ginseng (KRG) inhibited the expression of cyclooxygenase-2 (COX-2) by hypoxia via peroxisome proliferator–activated receptor gamma (PPARγ). The aim of the current study was to evaluate the possibility of ginsenoside Rf as an active ingredient of KRG in the inhibition of hypoxia-induced COX-2 via PPARγ. METHODS: The effects of ginsenoside Rf on the upregulation of COX-2 by hypoxia and its antimigration effects were evaluated in A549 cells. Docking of ginsenoside Rf was performed with the PPARγ structure using Surflex-Dock in Sybyl-X 2.1.1. RESULTS: PPARγ protein levels and peroxisome proliferator response element promoter activities were promoted by ginsenoside Rf. Inhibition of COX-2 expression by ginsenoside Rf was blocked by the PPARγ-specific inhibitor, T0070907. The PPARγ inhibitor also blocked the ability of ginsenoside Rf to suppress cell migration under hypoxia. The docking simulation results indicate that ginsenoside Rf binds to the active site of PPARγ. CONCLUSIONS: Our results demonstrate that ginsenoside Rf inhibits hypoxia induced-COX-2 expression and cellular migration, which are dependent on PPARγ activation. These results suggest that ginsenoside Rf has an antiinflammatory effect under hypoxic conditions. Moreover, docking analysis of ginsenoside Rf into the active site of PPARγ suggests that the compound binds to PPARγ in a position similar to that of known agonists.
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spelling pubmed-64375532019-04-11 Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells Song, Heewon Park, Joonwoo Choi, KeunOh Lee, Jeonggeun Chen, Jie Park, Hyun-Ju Yu, Byeung-Il Iida, Mitsuru Rhyu, Mee-Ra Lee, YoungJoo J Ginseng Res Research Article BACKGROUND: Ginsenoside Rf is a ginseng saponin found only in Panax ginseng that affects lipid metabolism. It also has neuroprotective and antiinflammatory properties. We previously showed that Korean Red Ginseng (KRG) inhibited the expression of cyclooxygenase-2 (COX-2) by hypoxia via peroxisome proliferator–activated receptor gamma (PPARγ). The aim of the current study was to evaluate the possibility of ginsenoside Rf as an active ingredient of KRG in the inhibition of hypoxia-induced COX-2 via PPARγ. METHODS: The effects of ginsenoside Rf on the upregulation of COX-2 by hypoxia and its antimigration effects were evaluated in A549 cells. Docking of ginsenoside Rf was performed with the PPARγ structure using Surflex-Dock in Sybyl-X 2.1.1. RESULTS: PPARγ protein levels and peroxisome proliferator response element promoter activities were promoted by ginsenoside Rf. Inhibition of COX-2 expression by ginsenoside Rf was blocked by the PPARγ-specific inhibitor, T0070907. The PPARγ inhibitor also blocked the ability of ginsenoside Rf to suppress cell migration under hypoxia. The docking simulation results indicate that ginsenoside Rf binds to the active site of PPARγ. CONCLUSIONS: Our results demonstrate that ginsenoside Rf inhibits hypoxia induced-COX-2 expression and cellular migration, which are dependent on PPARγ activation. These results suggest that ginsenoside Rf has an antiinflammatory effect under hypoxic conditions. Moreover, docking analysis of ginsenoside Rf into the active site of PPARγ suggests that the compound binds to PPARγ in a position similar to that of known agonists. Elsevier 2019-04 2018-11-30 /pmc/articles/PMC6437553/ /pubmed/30976170 http://dx.doi.org/10.1016/j.jgr.2018.11.007 Text en © 2018 The Korean Society of Ginseng, Published by Elsevier Korea LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Song, Heewon
Park, Joonwoo
Choi, KeunOh
Lee, Jeonggeun
Chen, Jie
Park, Hyun-Ju
Yu, Byeung-Il
Iida, Mitsuru
Rhyu, Mee-Ra
Lee, YoungJoo
Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells
title Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells
title_full Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells
title_fullStr Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells
title_full_unstemmed Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells
title_short Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in A549 cells
title_sort ginsenoside rf inhibits cyclooxygenase-2 induction via peroxisome proliferator–activated receptor gamma in a549 cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6437553/
https://www.ncbi.nlm.nih.gov/pubmed/30976170
http://dx.doi.org/10.1016/j.jgr.2018.11.007
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