title: The procyanidin trimer C1 inhibits LPS-induced MAPK and NF-κB signaling through TLR4 in macrophages.
abstract: Natural products and dietary components rich in polyphenols have been shown to reduce inflammation; however, the molecular mechanisms underlying this anti-inflammatory activity are not completely characterized, and many features remain to be elucidated. This research was carried out to clarify the potential role of procyanidin trimer C1 in the anti-inflammatory effect of polyphenols. Procyanidin C1 inhibited inducible nitric oxide synthase-mediated nitric oxide production and the release of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) in lipopolysaccharide (LPS)-induced macrophages. Treatment with procyanidin C1 resulted in a significant decrease in prostaglandin E2 and cyclooxygenase-2 levels, as well as the expression of cell surface molecules (CD80, CD86, and MHC class II), which was induced by LPS. Furthermore, our data demonstrated that the anti-inflammatory effect of procyanidin C1 occurs through inhibition of mitogen-activated protein kinase (p38 and c-Jun N-terminal kinase) and nuclear factor-κB signaling pathways. These 2 factors play a major role in controlling inflammation, through toll-like receptor 4, suggesting that procyanidin C1 plays a potent role in promoting anti-inflammatory activity in macrophages. These results represent a novel and effective therapeutic intervention for the treatment of inflammatory disease.
authors.affiliation: Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 580-185, Republic of Korea.
authors.forename: Eui-Baek
authors.initials: EB
authors.lastname: Byun
authors.forename: Nak-Yun
authors.initials: NY
authors.lastname: Sung
authors.forename: Eui-Hong
authors.initials: EH
authors.lastname: Byun
authors.forename: Du-Sup
authors.initials: DS
authors.lastname: Song
authors.forename: Jae-Kyung
authors.initials: JK
authors.lastname: Kim
authors.forename: Jong-Heum
authors.initials: JH
authors.lastname: Park
authors.forename: Beom-Seok
authors.initials: BS
authors.lastname: Song
authors.forename: Sang-Hyun
authors.initials: SH
authors.lastname: Park
authors.forename: Ju-Woon
authors.initials: JW
authors.lastname: Lee
authors.forename: Myung-Woo
authors.initials: MW
authors.lastname: Byun
authors.forename: Jae-Hun
authors.initials: JH
authors.lastname: Kim
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D015703:Antigens, CD / Q000378:metabolism; D044946:Biflavonoids / Q000494:pharmacology*; D002392:Catechin / Q000494:pharmacology*; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy*; D008070:Lipopolysaccharides / Q000276:immunology; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000235:genetics; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D044945:Proanthocyanidins / Q000494:pharmacology*; D051197:Toll-Like Receptor 4 / Q000276:immunology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015703:Antigens, CD; D044946:Biflavonoids; D008070:Lipopolysaccharides; D016328:NF-kappa B; D044945:Proanthocyanidins; D051197:Toll-Like Receptor 4; D009569:Nitric Oxide; C479583:procyanidin C; D002392:Catechin; D051546:Cyclooxygenase 2; D015232:Dinoprostone