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作 者:缪丽莉[1] 周爱玲[1] 朱燕[1] 施海燕[1]
机构地区:[1]南通大学,江苏南通226001
出 处:《时珍国医国药》2009年第3期581-583,共3页Lishizhen Medicine and Materia Medica Research
基 金:江苏省自然科学基金项目(No.BK2004048);江苏省高校自然科学基础研究项目(No.06KJB360085);南通大学自然科学研究项目(No.06z099)
摘 要:目的通过建立阿尔茨海默病(Alzheimer's disease,AD)大鼠模型,观察脑益康对AD大鼠学习记忆能力、β淀粉样前体蛋白(β-amyloid precursor protein,β-APP)裂解途径的影响,探讨脑益康改善AD模型大鼠症状的机制。方法采用β淀粉样蛋白毒性片段-(β-amyloid protein25-35,Aβ25-35)海马注射建立AD大鼠模型,用电迷宫刺激器检测大鼠学习记忆能力;免疫组织化学方法观察大鼠脑组织Aβ40/42表达的变化;逆转录-聚合酶链式反应(reverse transcription poly-merase chain reaction,RT-PCR)方法检测大鼠海马β-APPmRNA表达情况;Western-Blot方法测定大鼠皮层组织β位点剪切酶(β-amyloid precursor protein cleaving enzyme,BACE1)的表达。结果脑益康能提高AD模型大鼠的学习、记忆能力;抑制AD大鼠脑组织Aβ40/42的生成;下调AD大鼠海马β-APPmRNA的表达;减少AD大鼠脑皮层内BACE1蛋白的含量。结论脑益康减少脑内Aβ的沉积可能是通过抑制BACE1从而下调β-APP的表达而实现的。Objective To establish the animal model of Alzheimer's disease (AD) and to observe the effect of Nao Yikang on learning and memory ability of AD rats and its mechanisms. Methods The rat model was established by microinjection of Aβ25 -35 into bilateral hippocampus. The ability of learning and memory was tested by Y - maze. The expression of Aβ40/42 in AD rat brain was detected by immunohistochemistry. The expression of β - APP mRNA in hippocampus was detected by reverse transcription polymerase chain reaction( RT - PCR). Protein quantification for β- amyloid precursor protein cleaving enzyme ( BACE1 ) in cortex of AD rats was assessed by Western - blot analysis. Results Learning and memory ability of rats injected bilaterally with Aβ25-35 was decreased obviously,whereas Nao Yikang could improve the ability, inhibit the expression of Aβ40/42, β - APP mRNA and BACE1 protein. Conclusion Nao Yikang may decrease the Aβ deposition by inhibiting BACE1 to down - regulate the expression of β - APP.
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