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Anti‐inflammatory effect of wood‐cultivated ginseng in LPS‐stimulated RAW264.7 cells
Author(s) -
JEONG JIN BOO
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.lb623
Subject(s) - ginseng , nitric oxide , inflammation , western blot , araliaceae , chemistry , iκbα , biochemistry , nf κb , pharmacology , biology , signal transduction , microbiology and biotechnology , medicine , endocrinology , immunology , gene , alternative medicine , pathology
Ginseng ( Panax ginseng ) has been reported to exert an anti‐inflammatory activity in a variety of inflammatory. However, inflammation‐regulatory activity of wood‐cultivated ginseng has not been thoroughly evaluated. In this study, we evaluated the anti‐inflammatory effect of wood‐cultivated ginseng and elucidated the potential mechanisms in LPS‐stimulated RAW264.7 cells. Inhibitory effects of the old wood‐cultivated ginseng (WCG‐O), young wood‐cultivated ginseng (WCG‐Y) and ginseng (G) on NO and PGE 2 production were examined using the Griess assay and ELISA kit. Suppressive effects of WCG‐O on inflammatory gene expression, transcriptional activation, and inflammation signaling events were investigated using Western blot analysis, RT‐PCR analysis and luciferase activity reporter gene assay. WCG‐O dose‐dependently suppressed nitric oxide (NO) and Prostaglandin E 2 (PGE 2 ) production in LPS‐stimulated RAW264.7 cells. In addition, WCG‐O attenuated LPS‐mediated overexpression of iNOS and COX‐2. In addition, WCG‐O blocked the expression of TNF‐α and IL‐1β in LPS‐stimulated RAW264.7 cells. In elucidation of the potential mechanisms for anti‐inflammatory effect, WCG‐O inhibited the activation of IκK‐α/β, the phosphorylation of IκB‐α, and degradation of IκB‐α, which results in the inhibition of p65 nuclear accumulation and NF‐κB activation. In addition, WCG‐O suppressed the activation of ERK1/2, p38 and JNK, which results in the inhibition of ATF2 nuclear accumulation. These results indicate that WCG‐O may exert anti‐inflammatory activity through the inhibiting NF‐κB and MAPK signaling. From these findings, WCG‐O has potential to be a candidate for the development of chemoprevention or therapeutic agents for the inflammatory diseases. Support or Funding Information This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF‐2016R1D1A3B03931713). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .