|
KMID : 0352720070310040181
|
|
Journal of Ginseng Research
2007 Volume.31 No. 4 p.181 ~ p.190
|
|
|
Compound K (CK) Rich Fractions from Korean Red Ginseng Inhibit Toll-like Receptor (TLR) 4- or TLR9-mediated Mitogen-activated Protein Kinases Activation and Pro-inflammatory Responses in Murine Macrophages
|
|
Yang Chul-Su
Ko Sung-Ryong
Cho Byung-Goo
Lee Ji-Yeon
Kim Ki-Hye
Shin Dong-Min
Yuk Jae-Min
Sohn Hyun-Joo
Kim Young-Sook
Wee Jae-Joon
Do Jae-Ho
Jo Eun-Kyung
|
|
|
Abstract
|
|
|
|
Compound K (CK), a protopanaxadiol ginsenoside metabolite, was previously shown to have immunomodulatory effects. In this study, we isolated the CK rich fractions (CKRF) from Korean Red Ginseng and investigated the regulation of CKRF-mediated inflammatory signaling during Toll-like receptor (TLR)-mediated cellular activation. Among various TLR ligands, CKRF considerably abrogated TLR4- or TLR9-induced inflammatory signaling. Both LPS and CpG-containing oligodeoxynucleotides (CpG-ODN) stimulation rapidly activates mitogen-activated protein kinases [MAPKs; extracellular signal-regulated kinases ½ and p38], NF-κB, and expression of pro-inflammatory cytokines tumor necrosis factor-α and interleukin-6 in murine bone marrow-derived macrophages (BMDMs) in a time- and dosedependent manner. Of interest, pre-treatment of CKRF in either LPS/TLR4- or CpG-ODN/TLR9-stimulated macrophages substantially attenuated the LPS-induced inflammatory cytokine production and mRNA expressions, as well as MAPK and NF-κB activation. To our knowledge, this is the first description of the inhibitory roles for CKRF in TLR4- or TLR9- associated signaling in BMDMs. Collectively, these results demonstrate that CKRF specifically modulates distinct TLR4- and TLR9-mediated inflammatory responses, and further studies are urgently needed for their in vivo roles for potential therapeutic uses, such as in systemic inflammatory syndromes
|
|
|
KEYWORD
|
|
|
Compound K-rich fractions, Toll-like receptors, Mitogen-activated protein kinases, Inflammation
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|