The Effect Of Genistein On Learning And Memory Capacity And Antioxidant Effects And Expression Of AD7c-NTP In AD Model Mice

BackgroundAlzheimer’s Disease(AD) is a fatal progressive neurodegenerative disease. AD’s clinical manifestations are progressive decline of daily living activities, memory and cognitive function continues to deteriorate, with a variety of behavioral disorders and neuropsychiatric symptoms. Cerebrovascular disease, Cerebral degeneration, dysbolismus, genetic factor, drugs, tumor and so on, can cause AD. Amyloid precusor protein, apoproteinε4,α2-macroglobulin, protein Tau. and so on. can cause the development of AD and dementia. The main clinical manifestation is progressive mental status decay, as: analytical judgement ability decline, long-term and recent memory disability, behavioral disorder, emotion alteration, confusion, and so on. Because the body ceaseless contact with the outside, there are multiple factors, including the ceaseless respiration(oxidizing reaction), radiographic exposure, and so on, can continue to produce abundant free radicals. The study found that there are important links between oxidative stress disorder and the formation of AD, the oxidative stress disorder of AD patients occurs before the formation of AD. Genistein (GEN) has a good antioxidant capacity in many ways. ObjectiveTo investigate the effect of genistein on learning and memory capacity and antioxidant effects and expression of AD7c-NTP in AD model. Method40 mice were selected by intraperitoneal injection 120 mg/kg/d 1.2% D-Galactose and 200 mg/kg 0.9% sodium benzoate, gastric infusion 0.5ml / d 20mg/mlAlC13 solution.28 days.10 healthy mice as normal control group, the control group did not receive any treatment. MORRIS water maze test on the Day 6 after the establishment of the model, The difference between the average escape latency and the reference value representing the ratio of the average escape latency time of the mice>20% said modeling positive. Thirty positive mice were randomly divided into three groups.-model group(MG), high dose group (GEN-H:50mg/kg) and low dose group (GEN-L:10mg/kg). Gastric infusion on the seventh Day 7 after the establishment of the model, once ADay,28 days. The model group was given normal saline in the same time every day. SOD activity T-AOC total antioxidant capacity and MDA were observed in the cerebral cortex. AD7c-NTP immunohistochemistry and the expression levels of immunofluorescence were observed in the hippocampus.ResultAfter the intervention of GEN:The escape latency was significantly decreased (P< 0.05), the number of cross platform was significantly increased (P<0.01), SOD activity T-AOC total antioxidant capacity were increased (P<0.01); the AD7c-NTP positive cell were fusiform or star by immunohistochemistry. The AD7c-NTP positive cell and cell shADing in the hippocampus in the GEN-H group and GEN-L group were significantly decreased as compared with those in the model group (P<0.01). Immunofluorescence showed that the number of green fluorescent cells in the control group were significantly decreased as compared with those in the model group (P<0.01). The hippocampus hAD a visible green fluorescence in the GEN-H group and GEN-L group, but the number of cells were significantly decreased as compared with those in the model group (P<0.01)Conclusion1.Genistein can against the aging of the nervous system, improving learning and memory ability in mice.2.The mechanism of genistein were possible with increase SOD activity and T-AOC total antioxidant capacity, decrease the MDA content, inhibition of expression of AD7c-NTP.