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灵芝多糖肽对阿尔茨海默病大鼠β淀粉样蛋白含量和tau蛋白过度磷酸化的影响 被引量:15

Influence of ganoderma lucidum polysaccharides peptide on β-amyloid peptide and taus hyperphosphorylation in rat with Alzheimers disease
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摘要 目的观察灵芝多糖肽(ganoderma lucidum polysacchraride peptide,GLPP)对阿尔茨海默病大鼠空间记忆能力、海马β淀粉样蛋白(βamyloid petide,Aβ)含量、tau蛋白磷酸化及超微结构的影响及机制。方法雄性Wistar大鼠48只,随机分为对照组、模型组、生理盐水组、GLPP组各12只。除对照组(正常昼夜节律)外,其余各组连续光照(光照度400Lux,24h)30d,光照期间GLPP组灌胃质量分数2.5%GLPP 250mg/kg,生理盐水组灌胃相同体积生理盐水,均1次/d。光照30d后,采用Morris水迷宫试验检测大鼠空间记忆能力,采用放射免疫法检测大鼠海马Aβ含量,采用免疫组织化学法检测海马tau蛋白磷酸化水平,应用透射电镜观察海马超微结构改变。结果模型组和生理盐水组大鼠寻找平台潜伏期[(32.96±5.52)、(35.55±6.28)s]、海马Aβ含量[(66.12±1.81)、(63.54±1.17)ng/L]、海马tau蛋白在Ser396/Ser404(PHF-1位点)(42.60±3.91、39.82±3.78)和Ser199/Ser202(tau-1位点)(28.71±3.45、27.43±2.27)发生过度磷酸化阳性细胞数明显高于对照组[(12.95±2.48)s,(39.62±2.71)ng/L、28.73±2.99、21.03±2.73]和GLPP组[(14.29±3.31)s,(40.89±3.13)ng/L、30.80±4.38、22.64±2.81](P<0.05),模型组与生理盐水组比较差异无统计学意义(P>0.05);透射电镜结果显示,对照组和GLPP组大鼠海马组织超微结构正常,模型组和生理盐水组大鼠海马组织线粒体肿胀,线粒体嵴模糊或消失,结构破坏,神经突触减少甚至缺失,突触间隙模糊,突触小泡数量减少。结论 GLPP可使持续光照导致的阿尔茨海默病大鼠海马Aβ水平降低,抑制tau蛋白过度磷酸化,减轻超微结构的损伤,提高大鼠空间记忆能力。 Objective To observe the influence of ganoderma lucidum polysaccharides peptide (GLPP) on spatial memory, β-amyloid peptide (Aβ) content, tau's hyperphosphorylation and uhrastructure in hippocampus in rats with Alzheimer's disease. Methods Forty-eight male Wistar rats were randomly divided into four groups, control group, model group, normal saline group and GLPP group, with 12 rats in each group. Except control group (receiving 12 :12 light-dark cycle), the other three groups received continuous illumination (400 Lux illuminance for 24 h) totally for 30 days. During the illumination period, GLPP group received 2.5% GLPP 250 mg/kg, once a day, and normal saline group received the same volume normal saline once a day. After illumination for 30 days, spatial memory was detected by Morris water maze test, Aβ content was detected by radioimmunity method, and tau phosphorylation level was detected by immunohistochemistry, and ultrastrueture in hippocampus was observed on transmission electron microscope. Results The escape latency, Aβ content, the positive cells of phosphorylation tau protein in Ser396/Ser404 (PHF-1) site and Ser199/Ser202 (tau-1 site) were (32. 96±5. 52) s, (66. 12±1. 81) ng/L, 42. 60±3. 91 and 28. 71±3.45 in model group, and (35.55±6.28) s, (63.54±1.17) ng/L, 39.82±3.78 and 27.43±2.27 in normal saline group, significantly higher than those in control group ((12. 95±2. 48) s, (39.62±2.71) ng/L, 28.73±2. 99, 21.03±2.73) and GLPP group ((14.29±3.31) s, (40.89±3.13) ng/L, 30.80±4.38, 22.64±2.81) (P〈0.05), and there were no significant differences between model group and normal saline group (P〉0.05). Transmission electron microscope showed normal ultrastrueture in control group and GLPP group, and showed swell mitoehondria, vague or disappeared mitocbondrial crista, disorganized structure, reduced even missed synapses, fuzzy synaptic cleft and reduced number of synaptic vesicles in model group and normal
出处 《中华实用诊断与治疗杂志》 2015年第9期862-865,共4页 Journal of Chinese Practical Diagnosis and Therapy
基金 河南省医学科技攻关项目(200803094) 河南省教育厅自然科学项目(2009C310004)
关键词 阿尔茨海默病 灵芝多糖肽 β淀粉样蛋白 TAU蛋白 过度磷酸化 海马超微结构 空间记忆 Alzheimer's disease ganoderma lueidum polysaccharides peptide β-amyloid peptide tau protein hyperphosphorylation hippocampus ultrastructure spatial memory
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