Molecular mechanism of protopanaxadiol saponin fraction-mediated anti-inflammatory actions

• DOI: 10.1016/j.jgr.2014.06.002
• Publication Date: 2014-06-19T02:01:17Z
• Authors: Yanyan Yang; Jongsung Lee; Man Hee Rhee; Tao Yu; Kwang-Soo Baek; Nak Yoon Sung; Yong Kim; Keejung Yoon; Ji Hye Kim; Yi-Seong Kwak; Sungyoul Hong; Jong-Hoon Kim; Jae Youl Cho
• Keywords: Protopanaxadiol; Proinflammatory cytokine

Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only few studies have explored the molecular mechanism of KRG-mediated activity. We investigated mechanisms protopanaxadiol saponin fraction (PPD-SF) KRG using in vitro vivo inflammatory models. PPD-SF dose-dependently diminished release mediators [nitric oxide (NO), tumor necrosis factor-α, prostaglandin E2], downregulated mRNA expression their corresponding genes (inducible NO synthase, cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression these events appeared to be regulated by blockade p38, c-Jun N-terminal kinase (JNK), TANK (TRAF family member-associated NF-kappa-B activator)-binding 1 (TBK1), which are linked activation activating transcription factor 2 (ATF2) interferon regulatory 3 (IRF3). Moreover, this also ameliorated HCl/ethanol/-induced gastritis via phospho-JNK2 levels. These results strongly suggest that action could mediated reduction p38-, JNK2-, TANK-binding-kinase-1-linked pathways factors (ATF2 IRF3).