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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.