title: Chrysin suppresses LPS-stimulated proinflammatory responses by blocking NF-κB and JNK activations in microglia cells.
abstract: Neuroinflammation mediated by microglia has been implicated in neurodegenerative diseases. Suppression of microglial activation may therefore contribute to neuronal cell survival. Chrysin is present in honey and propolis and in low concentrations in fruits, vegetables, and certain beverages. It has been reported that chrysin has potent anti-inflammation, anti-cancer, and anti-oxidation properties. In the present study, we investigated the effects of chrysin on the production of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated microglia. Chrysin significantly inhibited the release of nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). The expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were also significantly inhibited by chrysin. Furthermore, chrysin inhibited the activations of c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB), which are signaling molecules involved in neuroinflammation. These results suggest that chrysin may act as a potential therapeutic agent for various neurodegenerative diseases involving neuroinflammation.
authors.affiliation: Graduate School of East-West Medical Science, Kyung Hee University Global Campus, #1 Seocheon-dong, Giheung-gu, Yongin, Gyeonggi-do 446-701, Republic of Korea.
authors.forename: Sang Keun
authors.initials: SK
authors.lastname: Ha
authors.forename: Eunjung
authors.initials: E
authors.lastname: Moon
authors.forename: Sun Yeou
authors.initials: SY
authors.lastname: Kim
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002460:Cell Line; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors; D004591:Electrophoresis, Polyacrylamide Gel; D004789:Enzyme Activation / Q000187:drug effects; D005419:Flavonoids / Q000494:pharmacology*; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors*; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D009569:Nitric Oxide / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D005419:Flavonoids; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; C043561:chrysin; D052247:Nitric Oxide Synthase Type II; D048031:JNK Mitogen-Activated Protein Kinases