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Protective Effects Of Selenium And Zinc To Senile Dementia Model

Posted on:2017-05-22Degree:MasterType:Thesis
Country:ChinaCandidate:C XuFull Text:PDF
GTID:2284330488455947Subject:Health Toxicology
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Objective Selenium and zinc is rich essential trace elements in central nervous system, also play an important role in the maintence of the central nervous normal physiological functions.In this experiment mainly through the establishment of in vivo and in vitro experiments dementia model, to study the protective effects of selenium、 zinc on embryonic rat neuronal cell damage and neurotoxicity induced by anti-β amyloid (Aβ25-35), and the dementia model mice learning memory impairment and change of biochemical index of brain tissue.Method In vitro experiment:The embryonic rat neurons with Aβ25-35 of 10 mol/L to induce AD model in vitro. The cell morphology methods, Thiazole blue colorimetric method(MTT), Lactate dehydrogenase (LDH)assays,Trace malondialdehyde (MDA) test,Hydrogen peroxide content test(H2O2),Nitric oxide content test(NO),western blot method to detect Glycogen synthase kinase-3β antibody (GSK-3β) and phosphorylated Tau protein (Ph-Tau) level.In vivo experimentation:60 male kunming mice, weight 18-20 g, randomly grouped into six groups,10 rats in each group. The dosage of 0.1 mol/10 g per mouse. the model of dementia mouse were made by intraperitoneal injection of D-gal 100 mg/Kg for 50 days. Gastric gavage selenium, zinc, canister to 45 days in a row, a total of 50 days experiment time. Observing animals every day. Using experiments of step-down test, step through test, shuttle box test to observe the ability of learning and memory in mice, MDA level, activities of TChE, MAO in the brain tissue of mouse.Results In vitro experiment:Aβ25-35 Injury group compared with control group,MTT metabolic rate decline,LDH quantity of release to increase,The content of H2O2 and NO and MDA increased,GSK-3βand Ph-Tau protein level increased, selenium and zinc and common set of selenium and zinc can Reduce cell toxicity induced by Aβ25-35 in different degrees,Selenium have significant protective effect.In vivo experimentation:The model group mice than other groups,Step through test appeared to show that the latent period were statistically shorten and wrong number were increased.In shuttle box test the latent period were statistically shorten and passive evading time of the high, the latent period were shorten statistically and errors rate were increased in Step-down test. The contents of MDA and the activated of AchE and MAO were increases statistically from brain tissue of the model group. in consequence, selenium, zinc can improve the learning and memory disorder, and the changes in MAO, AchE, MDA on model of dementia mouse.Conclusion The trace element selenium and zinc has markedly protective effect on the embryonic rat neuronal cell damage and neurotoxicity induced by A025-35-selenium, zinc can improve the learning and memory disorder, and the changes in MAO, AchE, MDA on model of dementia mouse, therefore, selenium, zinc can protect the alzheimer’s disease.
Keywords/Search Tags:Selenium,zinc, Alzheimer’s disease, Learning and memory disorders, Aβ25-35, MAO, MDA, TchE, GSK3β, Ph-Tua
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