Genistein Inhibited Amyloid-β induced Inflammatory Damage in C6 Glial Cells

Background and Aims. beta-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. We undertook this study to investigate the effects of GEN on inflammation induced by beta-amyloid25-35 treatment and the possible molecular mechanisms in C6 glial cells. Methods. C6 cells were pre-incubated with GEN for 2 h followed by the incubation with beta-amyloid 25-35 (A beta 25-35) for another 24 h. Inflammatory factors were detected by ELISA. The mRNA and protein expression of nuclear factor kappa B (NF-kappa B) p65 was measured using RT-PCR and Western blot, respectively. After inhibiting the NF-kappa Bp65 mRNA expression by using short interfering RNAs (siRNAs) technique, the changes of inflammatory factors levels were detected again. Results. GEN inhibited the production of inflammatory factors induced by A beta 25-35 treatment. A beta 25-35 treatment had no effect on the mRNA expression of NF-kappa Bp65 but upregulated the protein expression of NF-kappa Bp65. However, this upregulation effect on NF-kappa Bp65 protein expression was alleviated by GEN pretreatment. After inhibiting NF-kappa Bp65 mRNA expression by using siRNA technique, the effects of A beta 25-35 or GEN on the inflammatory factor generation were inhibited. Conclusions. These results indicated that GEN exhibited anti-inflammatory effects through regulating NF-kappa B signaling pathway in A beta 25-35-treated C6 glial cells. (C) 2014 IMSS. Published by Elsevier Inc.