Dissertation > Medicine, health > Chinese Medicine > Chinese medicine practitioners of other disciplines > TCM neurology and psychiatry

Protective Effects and Mechanism of Decoction of Polygonatum Against Learning and Memory Impairment Induced by Amyloid Beta-peptide in Rats

Author WangTaoTao
Tutor YaoYuYou
School Anhui Medical University,
Course Nutrition and Food Hygiene
Keywords polygonatum Alzheimer’s Disease Aβ25-35 learning and memory hippocampus P-tau
CLC R277.7
Type Master's thesis
Year 2013
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Objective To investigate the intervention effects of decoction ofpolygonatum(PCD) on Amyloid beta-peptide(Aβ)-induced Alzheimer’s Disease(AD) model and its mechanism in vivo and vitro.Methods To observe the effects of PCD on Aβ-induced AD model rats,40Sprague-Dawley(SD) rats were divided into4groups with10rats in each group. Group I was treated with saline as control; group Ⅱ was injected Aβ25-35into the CA1field of hippocampus as AD model, and group Ⅲ-Ⅳ, on the basis of the model, gavage administrated with low(15g/kg·d) or high(30g/kg-d) doses of PCD as treatment group. After intervention treatment for3weeks, the effects of PCD on learning and memory impariment on model rats were tested by Morris water maze; the effects of PCD on the activitives of glutathione peroxidase(GSH-Px), glutathione reductase(GR), total-superoxide dismutase(T-SOD) and levels of glutathione(GSH), malondialdehyde (MDA) in hippocampus of model rats were detected by biochemical assays. The effects of PCD on the histopathologic changes in CA1field of hippocampus in model rats were determined by histopathological method, and the effects of PCD on phospho-tau protein(P-tau) in CA1field of hippocampus on model rats was examined by immunohistechemical and western blot assays. The cytotoxic effects of Aβ25-35(0-30μM) on SH-SY5Y cells(SSC) was determined by MTT assay in vitro. In addition, the protective effects of PCD (20,40mg/mL) against Aβ25-35-induced neuronopathies and cytotoxic effects and its related mechanism were also investigated.Results1). Bilateral-injection Aβ25-35into the CA1region of adult SD rats under stereotaxic guidance induce AD model and cause the damage of the capacity of learning and memory and histopathologic change in brain of model rats.2). PCD (15,30g/kg) decreased the escape latency and swim distances of model rats, and improved the capacity of learning and memory. It is indicated that PCD possesses the protective effects aganist Aβ-induced learning and memory injury in rats.3). It is found that PCD (15,30g/kg) improved Aβ-induced histopathologic change in brain of model rats. H&E staining showed that PCD elevated neuron cells number in hippocampus, and reduced the range of nuclear pyknosis.4). Immunohistechemical and western blotting data showed that PCD (15,30g/kg) reduced the excessive expression of P-tau on the site of Thr231in CA1field of hippocampus in model rats.5). Biochemical assays showed that PCD (15,30g/kg) increased the activitives of GSH-Px, GR, SOD, and the level of GSH, whereas reduced the level of MDA, reducedthe degree of oxidative stress in hippocampus of model rats brain.6). In vitro, treatment with aggregated Aβ25-35(1-30μM) casued SSC injury and decreased cell viability in a concentration-dependent manner, and the IC50value of aggregated Aβ25-35is10μM. The viabilitives of the cells treated with PCD (20,40μg/mL) were increased significantly.Conclusion PCD possesses protective effects against the impairment of learning and memory in model rats. The protective mechanisms of PCD are highly ralated to eliminate reactive oxygen species (ROS), decrease the degree of oxidative stress, decrease the level of P-tau and inhibit cell damage induced by Aβ25-35.

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