| Objective:In composite Alzheimer’s disease (AD), animal models based on. The observation ofhuperzine A to improve the complex learning and memory ability of AD model rats andexplore the learning and memory huperzine A to improve the composite AD model rats,respectively, from the perspective of the serum oxidative stress indicators and brain cells,cyclin ability of possible mechanisms, and reveals part of the mechanism of ADpathogenesis and huperzine a possible mechanism to provide a new theoretical basis.Methods:(1) compound AD rat model of experimental groups: sham operation group, model groupand drug intervention group. Intraperitoneal injection of D-galactose Unitedintracerebroventricular injection of Aβ1-42complex model of AD; sham operation groupwith saline for placebo; drug intervention group after the model of huperzine A orally.(2) behavioral testing using the Morris water maze of rats in each group learning andmemory;(3) in the serum oxidative stress indexes in serum activities of SOD, MDA;(4) cycle-related proteins in the brain tissue by immunohistochemistry on brain tissue inthe cycle-related protein P53, P21detected.Results:(1) General condition and weight: animals in each group before modeling goodresponse, smooth hair, normal diet, quick action. Modeling the body weight of rats beganto reduce and slow action. Unresponsive, hair dry yellow, the lack of gloss,cheeks, hairremoval is obvious tail pigment spots, hyperpigmentation spotsincreased gradually deepen,lethargy. Intragastric administration of Huperzine A,abnormal behavior have differentlevels of relief such as the action becomes flexiblediet to promote hair than beforemoisturizing. (2) Morris water maze: rats in each group with the training times increase in latency.Compared with the sham operation group, model group, latency was significantlyprolonged (P <0.01), across the former platform significantly fewer (P <0.05) wasstatistically significant. Experiment1d, the drug group and model group, the incubationperiod compared to no significant difference (P>0.05);2-6d drug group compared withmodel group, the incubation period was significantly shorter (P <0.05), across the formerplatform the number was significantly increased (P <0.05); statistically significant.(3) in serum activities of SOD, the change of MDA results showed that: compared with thesham operation group, model group, SOD activity decreased significantly (P <0.01), MDAcontent increased significantly (P <0.01) were statistically significance; compared withmodel group, the SOD activity of the drug group was significantly higher content of MDAsignificantly reduced, with statistical significance (P <0.05).(4) by double immunofluorescence assay showed that: compared with the sham group,model group rat brain P53, P21positive cells increased significantly (P <0.01) wasstatistically significant. Compared with model group, drug group rat brain P53, P21positive cells decreased significantly (P <0.01) was statistically significant.Conclusion:(1) In this study, intraperitoneal injection of D-galactose and intracerebroventricularinjection of Aβ1-42, successful replication of the animal model of Alzheimer’s disease.The model is reproducible, reliable, is an ideal model of Alzheimer’s disease basic research.(2) Huperzine A may improve the composite model of AD in rats spatial learning andmemory ability.(3) Huperzine A can eliminate free radicals, improve antioxidant capacity, reduce brainfree radical damage to neurons；(4) Huperzine A has anti-apoptosis and protect neurons... |
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