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作 者:隋海娟[1] 马瑞国 刘卓[1] 闫恩志[1] 金英[1]
机构地区:[1]辽宁医学院药理学教研室,锦州121001 [2]锦州奥鸿药业有限责任公司,锦州121000
出 处:《中药药理与临床》2016年第2期71-73,共3页Pharmacology and Clinics of Chinese Materia Medica
基 金:辽宁省科学技术基金项目(2013022008)
摘 要:目的:研究知母皂苷(SAa B)对Aβ1-42诱导的大鼠学习记忆障碍的改善作用及机制。方法:选用SD大鼠48只随机分为4组:正常对照组,Aβ1-42组,SAa B(1、2.5 mg/ml)+Aβ1-42组,每组12只,侧脑室注射给药后第2 d进行Morris水迷宫实验,第7d快速取海马CA1区,Western Blot法观察磷酸化tau(P-tau)、磷酸化GSK-3β、磷酸化Akt蛋白及胆碱乙酰基转移酶(Ch AT)蛋白表达水平。结果:脑室内注射Aβ1-42大鼠出现明显的空间学习记忆障碍,表现为逃避潜伏期和游泳路程较正常对照组明显延长,在原平台象限游泳时间占总时间的百分比明显降低,同时伴有海马P-tau表达明显增加,p-GSK-3β、p-Akt、Ch AT表达明显降低。侧脑室内注射SAa B后,与Aβ1-42组相比,SAa B(1、2.5 mg/ml)+Aβ1-42组大鼠逃避潜伏期和游泳路程明显缩短,原平台象限游泳时间占总游泳时间百分比升高;海马P-tau表达明显降低,p-GSK-3β、p-Akt、Ch AT表达明显增加。结论:侧脑室内注射知母皂苷可通过降低Ptau表达水平,提高Ch AT活性,从而减少神经元纤维缠结的形成,并可能通过调节胆碱能功能的途径发挥抗痴呆的作用。Objective: To investigate the effect of saponins from Anemarrhena asphodeloides bge( SAa B) on Aβ1-42 induced on the learning and memory impairment in rats and the mechanisms. Methods: Forty-eight healthy male Sprague-Dawley( SD) rats were randomly divided into four groups: control group,Aβ1-42 group,SAa B( 1,2. 5 mg / ml) + Aβ1-42 group,n = 12. After intracerebroventricular injection of medication,second days Morris water maze test. Seventh days,fast cash in hippocampal CA1 region,Western blotting were used for phosphorylation of tau( p-tau),p-GSK-3β,p-Akt and choline acetyltransferase protein expression. Results: Injection after of Aβ1-42 single ventricles model,compared with the normal control group,the escape latency and swimming distance increased and percentage of time spent in the target quadrant lower( p 〈 0. 01),the expression of P-tau in hippocampus was significantly increased,p-GSK-3β,p-Akt and Ch AT expression decreased. After intraventricular injection of SAa B,compared with the Aβ1-42 group,SAa B( 1,2. 5 mg / ml) + Aβ1-42 significantly shorter escape latency and swimming distance,increase the percentage of time spent in the target quadrant( p 〈 0. 05,p 〈 0. 01); The expression of P-tau significantly decreased and p-GSK-3β,p-Akt,Ch AT significantly increased in the hippocampus of AD rats. Conclusion: SAa B can reduce the expression level of P-tau and increase the activity of Ch AT,thereby reducing the formation of neuronal fiber entanglement,and may antidementia by play a role in the regulation of cholinergic function.
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