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Effect of Ginsenoside Rb1 on Aβ and Related Protein Expression in Hippocampal Formation of Rats with Alzheimer’s Disease

Author: YangJiPing
Tutor: LaiHong
School: China Medical University
Course: Human Anatomy and Embryology
Keywords: Alzheimer 's disease (AD) Ginsenoside Rb1 (GSRb1) Hippocampal formation β- amyloid (Aβ) β-secretase (BACE) Early old prime -1 (PS-1)
CLC: R285.5
Type: Master's thesis
Year: 2008
Downloads: 220
Quote: 1
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Senile plaques of Alzheimer's disease (Alzheimer's disease, AD), one of the characteristic pathological changes, it is the core component of the β-amyloid (beta-amyloid, Aβ), while Aβ by β-amyloid precursor protein secretase enzyme (BACE) and γ-secretase cleavage. BACE is a key rate-limiting enzyme in the early old prime -1 (PS-1) can contribute to the synergistic effect of the BACE and γ-secretase enzyme, resulting in the generation amount of Aβ significantly increased Aβ production. Currently considered, PS-1 itself is composed of the most important part of the γ-secretase enzyme complex. Thus, by changing the BACE and the amount of the expression of PS-1 can directly regulate the level of Aβ. Ginseng is a traditional Chinese medicine of the puzzle, effective active ingredient ginsenoside (Ginsenoside, GS) excitatory effects on the central nervous system. Rb1 GS monomer components, is a diol saponins, neurotrophic, the role of to promote axon exogenous and nerve regeneration primary cultured hippocampal neurons and can significantly prolong the survival time. Recent years, studies have found GSRb1 inhibit hippocampal and cortical neurons induced by a variety of reasons hyperphosphorylation of tau protein significantly improved both the learning and memory abilities in a variety of experimental animals. However, GSRb1 AD molecular and biochemical changes in enzyme content is closely related to both Aβ production effect has not been reported in the literature. Therefore, the research through the establishment of the AD model observation Aβ, BACE and PS-1 expression in hippocampal structure changes, to further explore the pathogenesis of AD, at the same time comparing observed GSRb1 its expression. Materials and methods Experimental animals and groups: the selection of China Medical University Experimental Animal Center of Sprague-Dawley ♂ rats 45 (license number: SYXK [Liaoning] 2003-0013), weight 250g ± 20g, adaptive feeding 1w were randomly divided into three groups: control group, model group and treatment group. The model group ie 60mg · kg intraperitoneal injection of D-galactose -1 · d -1 and intragastric aluminum chloride 500mg · kg > · d -1 , qd for 60d; treatment group after intraperitoneal injection GSRb1 2.5mg · kg modeling end 1d -1 · d -1 , used in conjunction 4w; control group was given normal saline by intraperitoneal injection and gavage. Recent learning and memory in the Morris water maze behavioral test rats in each group, recorded each time period, the average escape latency. Suzuki silver staining method to observe pathological changes of the rat brain to determine whether the model is successful. Immunohistochemical staining observed the hippocampal structure distribution and expression of Aβ, BACE and PS-1-positive cells. 5, rats hippocampal structure BACE and PS-1 expression levels by Western blotting analysis. 6, combined with the image acquisition and analysis system, the resulting data are expressed as mean ± standard deviation ((?) ± 5), said application SPSS1 1.0 statistical software using one-way ANOVA for comparison between groups, P <0.05 as statistically significant. P <0.01 was considered significant statistically significant. Experimental results, the Morris water maze test results suggest that the model group rats each time period, the average incubation period is significantly longer than the control group (P <0.05) dose group compared with the model group, time period, the average incubation period was significantly shorter (P <0.05 ). 2, Suzuki silver staining the model rats cortex and hippocampal neurons neurofibrillary disorganized, twisting and aggregation obvious visible neurofibrillary tangles. While the control group showed the pathological changes. 3, immunohistochemistry results showed that Aβ 1-40 , BACE and PS-1 positive reaction product showed a brownish yellow or brown finely granular deposited mainly in the hippocampal CA1 region, CA3 region pyramidal cells layer and the granule cell layer of the dentate gyrus. The control group rat hippocampal structure can be seen that a small amount of AB 1-40 , BACE and PS-1-positive neurons; product coloring of the positive reaction of the model group than the control group deepened, integrated optical density (IOD) compared with The control group was significantly higher (P <0.01); treatment group of Aβ to 1-40 , BACE and PS-1 positive reaction products IOD compared with the model group decreased (P <0.05). 4, Western blotting results show that the model rats hippocampal structure BACE and PS-1 expression was significantly increased (P <0.01) than the control group. The hippocampal structure treatment group BACE and PS-expression levels relative to the model group was decreased (P <0.05). Conclusion AD hippocampal structure of Aβ, BACE and PS-1 expression than the control group were significantly increased. 2, treated rats hippocampal formation of Aβ, BACE and PS-1 expression in model group were significantly lowered. 3, D-galactose joint learning and memory impairment and pathological characteristics of aluminum trichloride is capable of simulating AD, is an ideal animal model drug screening AD treatment. 4, GSRb1 can significantly improve learning and memory impairment in AD rats, the mechanism may be by down-regulating hippocampal structure BACE and PS-1 abnormal expression, reducing the amount of Aβ generation, so as to reduce Aβ neurotoxicity.

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