Genistein inhibited β-amyloid25-35-induced inflammatory damage in C6 glial cells through regulating nuclear factor κBp65 signaling pathway
β-amyloid-induced inflammation has been implicated in the early pathologic events in neurodegenerative diseases.The anti-inflammation potential of genistein (GEN) had been proved recently in our previous studies.The present study was designed to investigate the efficacy of GEN on inhibiting β-amyloid25-35-induced inflammation and the possible molecular mechanisms in C6 glial cells.The C6 cells were pre-incubated with GEN for 2 h followed by the incubation with β-amyloid25-35 (Aβ25-35) for another 24 h.Inflammatory factors were detected by ELISA.The mRNA and protein expression of nuclear factor κB (NF-κB) p65 was measured by using RT-PCR and Western blot respectively.After inhibiting the NF-κ Bp65 mRNA expression by using short interfering RNAs (siRNAs) technique, the inflammatory factors levels were detected again.The results showed that GEN inhibited the production of inflammatory factors induced by Aβ25-35 treatment.Aβ25-35 treatment had no effect on the NF-κ Bp65 mRNA expression, but up-regulated the NF-κ Bp65 protein expression.While, this up-regulation effect on NF-κ Bp65 protein expression was alleviated by GEN pretreatment.After siRNA inhibit NF-κBp65 mRNA expression, the regulating effects of Aβ25-35 or GEN on the inflammatory factors were inhibited.These results suggested that GEN exhibited anti-inflammatory effects through regulating NF-κB signaling pathway in Aβ25-35-treated C6 glial cells.
Genistein Beta-amyloid peptides Inflammatory damage NF-κB siRNA
Xia Zhao Linhong Yuan Huanling Yu Yuandi Xi Weiwei Ma Xin Zhou Juan Ding Rong Xiao
Department of Nutrition and Food Hygiene, Capital Medical University, Beijing, PR China
国内会议
北京
英文
1-13
2013-11-01（万方平台首次上网日期，不代表论文的发表时间）