title: Soybean glyceollins mitigate inducible nitric oxide synthase and cyclooxygenase-2             expression levels via suppression of the NF-κB signaling pathway in RAW 264.7             cells.
abstract: Glyceollins, produced to induce disease resistance responses against specific species, such as an incompatible pathogen Phytophthora sojae in soybeans, have the potential to exhibit anti-inflammatory activity in RAW 264.7 cells. To investigate the anti-inflammatory effects of elicited glyceollins via a signaling pathway, we studied the glyceollin signaling pathway using several assays including RNA and protein expression levels. We found that soybean glyceollins significantly reduced LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production, as well as the expression of inducible ΝΟ synthase (iNOS) and cyclooxygenase-2 (COX-2) via the suppression of NF-κB activation. Glyceollins also inhibited the phosphorylation of IκBα kinase (IKK), the degradation of IκBα, and the formation of NF-κB-DNA binding complex in a dose-dependent manner. Furthermore, they inhibited pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-18, but increased the generation of the anti-inflammatory cytokine IL-10. Collectively, the present data show that glyceollins elicit potential anti-inflammatory effects by suppressing the NF-κB signaling pathway in RAW 264.7 cells.
authors.affiliation: Department of Food Science and Biotechnology, Kyungpook National                     University, Daegu 702-701, Republic of Korea.
authors.forename: Eun-Kyung
authors.initials: EK
authors.lastname: Yoon
authors.forename: Hyun-Kyoung
authors.initials: HK
authors.lastname: Kim
authors.forename: Song
authors.initials: S
authors.lastname: Cui
authors.forename: Yong-Hoon
authors.initials: YH
authors.lastname: Kim
authors.forename: Sang-Han
authors.initials: SH
authors.lastname: Lee
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D015153:Blotting, Western; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D060467:Disease Resistance; D051550:I-kappa B Kinase / Q000037:antagonists & inhibitors / Q000378:metabolism; D020672:I-kappa B Proteins / Q000378:metabolism; D020382:Interleukin-18 / Q000037:antagonists & inhibitors / Q000378:metabolism; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000378:metabolism; D051379:Mice; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology*; D036343:Pterocarpans / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects*; D013025:Glycine max / Q000737:chemistry*
chemical_list: D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D020382:Interleukin-18; D053583:Interleukin-1beta; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D010936:Plant Extracts; D036343:Pterocarpans; D000072000:NF-KappaB Inhibitor alpha; C017343:glyceollin; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D051550:I-kappa B Kinase