|
KMID : 0352720190430020319
|
|
Journal of Ginseng Research
2019 Volume.43 No. 2 p.319 ~ p.325
|
|
|
Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator?activated receptor gamma in A549 cells
|
|
Song Hee-Won
Park Joon-Woo
Choi Keun-Oh
Lee Jeong-Geun
Chen Jie
Park Hyun-Ju
Yu Byeung-Il
Iida Mitsuru
Rhyu Mee-Ra
Lee Young-Joo
|
|
|
Abstract
|
|
|
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.
|
|
|
KEYWORD
|
|
|
COX-2, ginsenoside Rf, hypoxia, PPARγ
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
|