title: Effects of ginsenoside Re on LPS-induced inflammatory mediators in BV2 microglial cells.
abstract: BACKGROUND
  Microglial activation plays an important role in neurodegenerative diseases by producing several pro-inflammatory enzymes and pro-inflammatory cytokines. Lipopolysaccharide (LPS)-induced inflammation leads to the activation of microglial cells in the central nervous system (CNS) and is associated with the pathological mechanisms of neurodegenerative diseases, including PD, AD, and ALS. Ginseng is a natural antioxidant used in herbal medicine and contains ginsenosides (Rb1, Rg1, Rg3, Re, and Rd), which have anti-neoplastic and anti-stress properties.This study demonstrates the involvement of the anti-inflammatory signaling pathway, ginsenoside-Re (G-Re), which is one of the ginsenosides mediated by LPS-induced neuroinflammation in BV2 microglial cells.
  
  
  METHODS
  BV2 microglial cells were pretreated with 2 μg/ml G-Re and stimulated with 1 μg/ml LPS to induce neuroinflammation. To investigate the effect of G-Re on LPS-induced cell signaling, we performed western blotting and immunofluorescence using specific antibodies, such as phospho-p38, COX2, and iNOS.
  
  
  RESULTS
  Pretreatment with 2 μg/ml G-Re was neuroprotective against 1 μg/ml LPS-treated microglial cells. The neuroprotective events induced by G-Re treatment in neuroinflammation occurred via the phospho-p38, iNOS, and COX2 signaling pathways in BV2 cells.
  
  
  CONCLUSIONS
  Taken together, we suggest that G-Re exerts a beneficial effect on neuroinflammatory events in neurodegenerative diseases.
authors.affiliation: Department of Medical Research, Korea Institute of Oriental Medicine, Yuseong-gu, Daejeon, Republic of Korea.
authors.forename: Kang-Woo
authors.initials: KW
authors.lastname: Lee
authors.forename: So Young
authors.initials: SY
authors.lastname: Jung
authors.forename: Sun-Mi
authors.initials: SM
authors.lastname: Choi
authors.forename: Eun Jin
authors.initials: EJ
authors.lastname: Yang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002460:Cell Line; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D019636:Neurodegenerative Diseases / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D005894:Panax / Q000737:chemistry*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D015398:Signal Transduction
chemical_list: D000893:Anti-Inflammatory Agents; D036145:Ginsenosides; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D018696:Neuroprotective Agents; D010936:Plant Extracts; C049864:ginsenoside Re