Genistein attenuates D-galactose-induced oxidative damage through decreased reactive oxygen species and NF-κB binding activity in neuronal PC12 cells.

摘要: Abstract Aims We investigated the mechanism of D-galactose (DG)-induced oxidative damage and neuroprotective action genistein in PC12 cells. Main methods cells were treated with 40 mM DG dissolved medium containing 85% RPMI1640, 10% HBS 5% FBS or without genistein. measured protein expression β-amyloid (Aβ), advanced glycation end products (AGEs), IκB-α manganese-superoxide dismutase (MnSOD) by western blotting, intracellular reactive oxygen species (ROS) 2, 7-dichlorofluorescin-diacetate, binding activity nuclear factor kappa B (NF-κB) electrophortic mobility shift assay. Key findings (40 mM) completely retarded cell growth after incubation for 72 h, this effect was not due to osmotic changes, as mannitol had no effect. Mechanistically, we found that increased ROS starting at 4 h Aβ AGEs 24 h. treatment 24 h also NF-κB but strongly decreased protein. Furthermore, 48 h MnSOD expression. All these effects effectively inhibited (0.5–10 μM). Significance The present study indicates protection against DG-induced stress cells, is likely mediated NF-κB.