Phenolic-rich fraction from Rhus verniciflua Stokes (RVS) suppress inflammatory response via NF-kappaB and JNK pathway in lipopolysaccharide-induced RAW 264.7 macrophages.
The effects of phenolic-rich fraction (PRF) from Rhus verniciflua Stokes (Anacardiaceae) on the activities of cellular signaling molecules that mediate inflammatory responses in LPS-induced RAW 264.7 macrophages were investigated. At various concentrations of PRF significantly inhibited NO, PGE(2) and TNF-alpha production in LPS-induced RAW 264.7 macrophage cells. The PRF also significantly inhibited iNOS and COX-2 protein expression in LPS-induced RAW 264.7 macrophage in a concentration-dependent manner. Transcription factor NF-kappaB plays a key role for the inducible expression of genes mediating proinflammatory effects and here, we show that PRF can inhibit the induction of NF-kappaB activity. The PRF effectively inhibited the iNOS and COX-2 protein expression through suppression of phospho-JNK1/2 activation. Study using PDA HPLC has found that the PRF contains several low molecular compounds (i.e. p-coumaric acid, fustin, kaempferol-3-O-glucoside, sulfuretin, butein, kaempferol). Our results indicate that the anti-inflammatory properties of PRF might result from the inhibition of pro-inflammatory mediators (e.g., NO, PGE(2) and TNF-alpha) by suppression of such signaling pathways as NF-kappaB and JNK1/2.
Jung
Chang Hwa
CH
Laboratory of Clinical Biology and Pharmacogenomics, College of Oriental Medicine, Kyunghee University, Seoul 130-701, Republic of Korea.
Kim
Ji Hye
JH
Hong
Myung Hee
MH
Seog
Ho Moon
HM
Oh
Seong Hoon
SH
Lee
Pan Jae
PJ
Kim
Gyung Jun
GJ
Kim
Hyung Min
HM
Um
Jae Young
JY
Ko
Seong-Gyu
SG
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival; D051546:Cyclooxygenase 2 / Q000187:drug effects; D015232:Dinoprostone / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects; D048031:JNK Mitogen-Activated Protein Kinases / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects; D010636:Phenols / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology*; D008517:Phytotherapy; D024301:Plant Bark; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology; D010946:Plants, Medicinal; D029045:Rhus / Q000737:chemistry*; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010636:Phenols; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D048031:JNK Mitogen-Activated Protein Kinases; D015232:Dinoprostone