• Xin Zhou, Linhong Yuan, Xia Zhao, Chengcheng Hou, Weiwei Ma, Huanling Yu, and Rong Xiao.
• 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.
• Nutrition. 2014 Jan 1;30(1):90-5.

ObjectivesMicroglia 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.MethodsBV-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.ResultsThe 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.ConclusionThese 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.Copyright © 2014 Elsevier Inc. All rights reserved.

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