Neuroprotective effects of genistein and folic acid against oxidative damage of beta amyloid 31-35-induced in rat cortical neurons

Genistein and folic acid have been reported to protect against the development of cognitive dysfunction. However, the underlying mechanism(s) for this protection remains unclear. In this report, the isolated and combined protective effects of genistein and folic acid on beta amyloid 31-35 (Aβ31-35) induced oxidative damage were investigated to explore the mechanism(s) by using rat cultured cortical neurons. Following the exposure of cortical neurons to Aβ31-35, the fluidity of cell membrane of cortical neurons, mitochondrial membrane poptential (MMP) and the relative value of GSH/GSSG were significantly decreased determined by fluorescence polarization, flow cytometer and GSH/GSSG assy kit respectively, while the percentage of comet cells, tail length and the levels of reactive oxygen specis (ROS) and Ca²⁺ in neurons were signifcantly increased investigated by single cell gel electrophoresis and laser scanning confocal microscope. We also found that genistein and folic acid, both separately and collaboratively, increased the fluidity of cell membrane of cortical neurons, MMP and the relative value of GSH/GSSG in Aβ 31-35-treated neurons, while decreased the percentage of comet cells, tail length and the levels of ROS and Ca²⁺ in Aβ 31-35 treated-neurons. Furthermore, a more significant reduction in tail length and a more significant increase in MMP were observed in the coadministered neurons comparing to genistein solo-treated neurons. All these results indicated that the neurotoxity of Aβ 31-35 maybe related to its oxidative damage activity and the protective effect of genistein and folic acid was achieved by alleviating the oxidative damage of Aβ 31-35 to rat cortical neurons and maintaining the balance of redox.