Neuro-protective Mechanism of Isoflavones on Senescence-accelerated Mice

AimTo investigate the neuro-protective mechanism of isoflavones, using senescence-accelerated SAM-P/8 mice.MethodsVarious 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.ResultsMice treated with isoflavones performed significantly better in the cognitive test than the no-treatment control group (P < 0.05). The cortex AchE activity, serum SOD and GSH-Px activities were notably higher than those of the untreated mouse (P < 0.05). MDA concentration and the β-secretase activity in the hippocampal tissue were both lower than those in no-treatment control (P < 0.05). The numbers of hippocampal neurons of isoflavones treatment mice were increased and the cellular morphology was significantly improved.ConclusionIsoflavones 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.