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  To explore the mechanism(s) of the neuroprotective effects of genistein(GEN) alone or combined effects with 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 2h prior to exposing to Aβ31-35.Cell viability and fluidity of cell membrane were measured by MTT and fluorescence polarization(FPIA),respectively.Intracellular ROS and Ca~(2+) concentrations were measured by laser scanning confocal microscope.GSH and GSSG in mitochondria were measured by enzymatic method.Flow cytometry technique was used to measure mitochondrial membrane potential(MMP).The expression of HCY-2 and p38-MAPK mRNA in neurons was analyzed by RT-PCR.Results showed GEN and/or FA increased cell viability,reduced concentration of Ca~(2+) and generation of ROS in neurons compared with Aβ31-35-treated cells.Furthermore,the ratio of GSH/GSSG in mitochondrial and MMP were increased after GEN and/or FA treatment.RT-PCR results showed GEN and/or FA down-regulated expression of HCY-2 and p38-MAPK mRNA. Conclusion 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 mitochondria membrane integrity and modulating the signal pathways related to oxidation and apoptosis.……