Neuro-protective Mechanism of Isoflavones on Senescence-accelerated Mice

Abstract Aim To investigate the neuro-protective mechanism of isoflavones, using senescence-accelerated SAM-P/8 mice. Methods Various dosages of isoflavones were intragastrically administered to SAM-P/8 senescence-accelerated mice. The cortex acetylcholinesterase (AchE) activity, serum superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were examined. In addition, the concentration of malondialdehyde (MDA) was examined. β-secretase activity in the hippocampus tissue was determined by fluorometry. Changes of the hippocampal neurons were observed under a light microscope. Results Mice treated with isoflavones performed significantly better in the cognitive test than the no-treatment control group ( P P P Conclusion Isoflavones can indirectly increase the concentration of the cholinergic neural transmitter Ach through regulation of AchE. Through reduction of hippocampal β-secretase activity, the strong anti-oxidative activity of isoflavones can decrease the formation and deposition of insoluable β-amyloid (Aβ) debris, relieve the resulting toxicity and damage to neurons, and thereby effectively protect the nervous system.