title: Capsaicin exhibits anti-inflammatory property by inhibiting IkB-a degradation in LPS-stimulated peritoneal macrophages.
abstract: Capsaicin, a major ingredient of hot pepper, was considered to exhibit an anti-inflammatory property. In order to clarify the signalling mechanism underlying the anti-inflammatory action of capsaicin, we investigated the effect of capsaicin on the production of inflammatory molecules in lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages. The level of PGE2 was measured by EIA. The expression levels of COX-2, iNOS, IkB-a, and vanilloid receptor-1 (VR-1) were determined at the protein and mRNA levels. Significant inhibition of the production of LPS-induced PGE2 by capsaicin was observed in a dose-dependent manner. Capsaicin did not affect the COX-2 expression at either the protein or mRNA level, but inhibited the enzyme activity of COX-2 and the expression of the iNOS protein. Capsaicin completely blocked LPS-induced disappearance of IkB-a and therefore inactivated NF-kB. The inhibitory action of capsaicin on PGE2 production was not abolished by capsazepine, a specific antagonist to VR-1. A high expression level of the VR-1 like protein (VRL-1) was observed in peritoneal macrophages, while the expression of VR-1 was not detected. These findings suggest that the anti-inflammatory action of capsaicin may occur through a novel mechanism, not by a VR-1 receptor-mediated one. Both capsaicin and capsazepine may be a promising drug candidates for ameliorating inflammatory diseases and cancer.
authors.affiliation: Department of Food Science and Nutrition, University of Ulsan, Mugeo-dong, Nam-ku, Ulsan 680-749, South Korea.
authors.forename: Chu-Sook
authors.initials: CS
authors.lastname: Kim
authors.forename: Teruo
authors.initials: T
authors.lastname: Kawada
authors.forename: Byung-Sam
authors.initials: BS
authors.lastname: Kim
authors.forename: In-Seob
authors.initials: IS
authors.lastname: Han
authors.forename: Suck-Young
authors.initials: SY
authors.lastname: Choe
authors.forename: Tadao
authors.initials: T
authors.lastname: Kurata
authors.forename: Rina
authors.initials: R
authors.lastname: Yu
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology*; D051546:Cyclooxygenase 2; D015232:Dinoprostone / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D015971:Gene Expression Regulation, Enzymologic; D020672:I-kappa B Proteins / Q000378:metabolism*; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D011955:Receptors, Drug / Q000235:genetics / Q000378:metabolism; D050916:TRPV Cation Channels
chemical_list: D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D007527:Isoenzymes; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D011955:Receptors, Drug; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D002211:Capsaicin