title: Anti-inflammatory effect of ginsenoside Rg5 in lipopolysaccharide-stimulated BV2 microglial cells.
abstract: Microglia are resident immune cells in the central nervous system. They play a role in normal brain development and neuronal recovery. However, overactivation of microglia causes neuronal death, which is associated with neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. Therefore, controlling microglial activation has been suggested as an important target for treatment of neurodegenerative diseases. In the present study, we investigated the anti-inflammatory effect of ginsenoside Rg5 in lipopolysaccharide (LPS)-stimulated BV2 microglial cells and rat primary microglia. The data showed that Rg5 suppressed LPS-induced nitric oxide (NO) production and proinflammatory TNF-α secretion. In addition, Rg5 inhibited the mRNA expressions of iNOS, TNF-α, IL-1b, COX-2 and MMP-9 induced by LPS. Further mechanistic studies revealed that Rg5 inhibited the phophorylations of PI3K/Akt and MAPKs and the DNA binding activities of NF-kB and AP-1, which are upstream molecules controlling inflammatory reactions. Moreover, Rg5 suppressed ROS production with upregulation of hemeoxygenase-1 (HO-1) expression in LPS-stimulated BV2 cells. Overall, microglial inactivation by ginsenoside Rg5 may provide a therapeutic potential for various neuroinflammatory disorders.
authors.affiliation: Department of Molecular Medicine and Tissue Injury Defense Research Center, Ewha Womans University Medical School, Seoul 110-783, Korea. hskimp@ewha.ac.kr.
authors.forename: Yu Young
authors.initials: YY
authors.lastname: Lee
authors.forename: Jin-Sun
authors.initials: JS
authors.lastname: Park
authors.forename: Ji-Sun
authors.initials: JS
authors.lastname: Jung
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Kim
authors.forename: Hee-Sun
authors.initials: HS
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000235:genetics; D015536:Down-Regulation / Q000187:drug effects; D036145:Ginsenosides / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000235:genetics; D008070:Lipopolysaccharides / Q000276:immunology*; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D017628:Microglia / Q000166:cytology / Q000187:drug effects* / Q000276:immunology* / Q000378:metabolism; D009569:Nitric Oxide / Q000276:immunology; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D036145:Ginsenosides; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C572381:ginsenoside Rg5; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D020780:Matrix Metalloproteinase 9