title: Genistein antagonizes inflammatory damage induced by β-amyloid peptide in microglia through TLR4 and NF-κB.
abstract: OBJECTIVE
  Microglia activation and neuroinflammation have been associated with the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). Toll-like receptor 4 (TLR4) and nuclear factor (NF)-κB-mediated signal pathways exert key modulating roles in the inflammatory processes. The aim of the present study was to investigate whether genistein (Gen) has a neuroprotective effect against inflammatory damage induced by β-amyloid peptide25-35 (Aβ25-35) through the TLR4 and NF-κB-mediated signal pathways.
  
  
  METHODS
  BV-2 microglia cells were preincubated with Gen for 2 h and then treated with 25 μM Aβ25-35 for another 24 h. The expression of inflammatory mediators, TLR4 and NF-κB and the activity of NF-κB were measured.
  
  
  RESULTS
  The results showed that Gen could attenuate the cytotoxicity and inflammatory damage induced by Aβ25-35. Gen also significantly reversed Aβ25-35-induced up-regulation of TLR4 and NF-κB expression and the DNA binding and transcriptional activities of NF-κB.
  
  
  CONCLUSIONS
  These results indicated that Gen could alleviate the inflammation caused by Aβ25-35 treatment, which might be associated with the regulation of the TLR4/NF-κB signal pathway.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Capital Medical University, Beijing, P.R. China; Department of Nutrition, Beijing Jishuitan Hospital, Beijing, P.R. China.
authors.forename: Xin
authors.initials: X
authors.lastname: Zhou
authors.forename: Linhong
authors.initials: L
authors.lastname: Yuan
authors.forename: Xia
authors.initials: X
authors.lastname: Zhao
authors.forename: Chengcheng
authors.initials: C
authors.lastname: Hou
authors.forename: Weiwei
authors.initials: W
authors.lastname: Ma
authors.forename: Huanling
authors.initials: H
authors.lastname: Yu
authors.forename: Rong
authors.initials: R
authors.lastname: Xiao
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000009:adverse effects*; D000818:Animals; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D019833:Genistein / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010446:Peptide Fragments / Q000009:adverse effects*; D015398:Signal Transduction / Q000187:drug effects*; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D016229:Amyloid beta-Peptides; D016328:NF-kappa B; D018696:Neuroprotective Agents; D010446:Peptide Fragments; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; C074636:amyloid beta-protein (25-35); D019833:Genistein
keywords: Genistein; NF-κB; Neuroinflammation; TLR4; β-amyloid peptides 25-35