Genistein and folic acid prevent oxidative injury induced by β-amyloid peptide.

To explore the mechanism(s) of the neuroprotective effects of genistein (GEN) and folic acid (FA) on neurons treated with beta amyloid 31-35 (Aβ31-35), the primary cultured cortical neurons were treated with GEN and/or FA for 2 hr prior to exposure to Aβ31-35. Cell viability and fluidity of cell membrane were measured by 3-[4,5-dimethylthiazol-2]-2,5 diphenyltetrazolium bromide and fluorescence polarization, respectively. Intracellular reactive oxygen species (ROS) and Ca(2+) concentrations were measured by laser scanning confocal microscope. Glutataione (GSH) and Glutathione disulfide (GSSG) in mitochondria were measured by enzymatic method. Flow cytometry technique was used to measure mitochondrial membrane potential. The expression of HCY-2 and p38-MAPK mRNA in neurons was analysed by reverse transcription-polymerase chain reaction (RT-PCR). The results showed that GEN and/or FA increased cell viability and reduced concentration of Ca(2+) and generation of ROS in neurons compared with Aβ31-35-treated cells. Furthermore, the ratio of GSH/GSSG in mitochondria and mitochondrial membrane potential was increased after GEN and/or FA treatment. RT-PCR results showed that GEN and/or FA down-regulated expression of HCY-2 and p38-MAPK mRNA. We conclude that GEN and/or FA had neuroprotective effects in Aβ31-35-treated neurons. The mechanisms might be associated with multiple factors such as maintaining redox balance, stabilizing mitochondrial membrane integrity and modulating the signal pathways related to oxidation and apoptosis.