Neuroprotection of soyabean isoflavone co-administration with folic acid against beta-amyloid 1-40-induced neurotoxicity in rats.

Soya isoflavones (SIF) and folic acid (FA) both confer the biological properties of antioxidation; however, the mechanism of their antioxidant effect on nervous system development is unclear. Our purpose is to investigate the neuroprotective effects of SIF, FA or co-administration of SIF with FA against beta-amyloid 1-40 (Abeta1-40)-induced learning and memory impairment in rats. In the present study, the learning and memory ability of rats and the amount of amyloid-positive neurons in the cerebral cortex and hippocampal CA1 area were measured. The levels of total antioxidant capacity (T-AOC), glutathione (GSH) and glutathione peroxidase (GSH-Px) in serum and brain tissue were also measured. The results showed that intracerebroventricular administration of Abeta1-40 resulted in a dramatic prolongation of the escape latency; however, in the SIF, FA and SIF+FA treatment groups, the functional deficits of learning and memory were significantly improved. Moreover, after Abeta1-40 injection, the levels of T-AOC and GSH were profoundly decreased, suggesting a decline of antioxidant activity in the rats. However, intragastric pre-treatment with SIF, or FA, or SIF+FA resulted in a significant increase of antioxidative activity. SIF, or FA, or SIF+FA treatments also reversed the Abeta1-40-induced increase in the amount of amyloid-positive neurons. These results suggest that: (1) learning or memory impairment in experimental rats was caused by Abeta1-40, which is probably attributed to Abeta-induced oxidative damage and deposition of beta-amyloid peptides in the brain; (2) pre-administration of SIF and/or FA may prevent the pathological alterations caused by Abeta1-40 treatment and the neuroprotective effects of SIF and/or FA are indicated.