OBJECTIVES: 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. CONCLUSION: 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.
OBJECTIVES: 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. CONCLUSION: 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: Alyria Teixeira Dias; Sandra Bertelli Ribeiro de Castro; Caio César de Souza Alves; Marcilene Gomes Evangelista; Luan Cristian da Silva; Daniele Ribeiro de Lima Reis; Marco Antonio Machado; Maria Aparecida Juliano; Ana Paula Ferreira Journal: Inflamm Res Date: 2018-04-23 Impact factor: 4.575
Authors: Kathrin Pfarr; Corina Danciu; Olga Arlt; Christina Neske; Cristina Dehelean; Josef M Pfeilschifter; Heinfried H Radeke Journal: PLoS One Date: 2015-03-10 Impact factor: 3.240