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作 者:陈地灵[1] 张鹏[2] 林励[2] 张鹤鸣[1] 刘颂豪[1]
机构地区:[1]华南师范大学药物研究院,广东广州510631 [2]广州中医药大学中药学院,广东广州510006
出 处:《中国中药杂志》2013年第9期1306-1309,共4页China Journal of Chinese Materia Medica
基 金:海南省重点科技计划项目(090603)
摘 要:目的:观察巴戟天低聚糖(oligosaccharides of Morinda officinalis,OMO)对Aβ25-35致SD大鼠拟痴呆模型的影响,阐明其治疗痴呆症的药效机制。方法:采用SD大鼠双侧海马区注射Aβ25-35各10μg制备拟痴呆模型,实验设置空白对照组、假手术组、模型组、阳性药安理申组(0.125 mg.kg-1.d-1)、OMO高、低剂量组(60,20 mg.kg-1.d-1)。手术后15 d开始连续给药25 d后,采用试剂盒-酶标仪法测定脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GSH-Px)、乙酰胆碱(ACh)、乙酰胆碱酯酶(AChE)以及Na+/K+-ATPase等水平。结果:与模型组比较,各给药组大脑组织中SOD,CAT,GSH-Px活力增加,MDA含量降低(P<0.01);各给药组乙酰胆碱水平升高,乙酰胆碱酯酶水平降低和脑能量代谢水平Na+/K+-ATPase活性升高。结论:OMO通过提高抗氧化能力、激活脑能量代谢、改善胆碱能系统损伤等作用以改善Aβ25-35致大鼠痴呆症状。Objective: To observe the effect of oligosaccharides of Morinda officinalis (OMO) on β-amyloid-induced dementia rats, and study its pharmacological mechanism in treatment of dementia. Method: The dementia model rats were established by injec- ting Aβ25-35 10 μg into bilateral hippocampus. OMO high-dose (60 mg · kg^-1· d^-1) group, OMO low-dose (20 mg · kg^-1· d^-1) groups, the blank group, the sham operation group and the positive donepezil HC1 group (0. 125 mg · kg^-1· d^-1) were designed for the experiment. They were continuously administered with drugs at the 152 day after operation for 25 days. Kit microplate method was used to detect the contents of super oxide dismutase ( SOD), malondialdehyde ( MDA), catalase ( CAT), glutathione reductase (GSH-Px), acetylcholine (ACh), acetylcholinesterase (ACHE) and Na +/K + -ATPase. Result: Compared with the model group, all of administration groups showed higher SOD, CAT and GSH-Px levels, and lower MDA in the brain tissues. Besides, they also showed rise in the activities of ACh and Na+/K + -ATPase. Conclusion: OMO can ameliorate on β-amyloid-induced dementia rats by enhan- cing oxidation resistance, activating brain energy metabolism and improving the injury of cholinergic system.
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