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:《中国药理学通报》2013年第2期271-276,共6页Chinese Pharmacological Bulletin
基 金:海南省重点科技项目(No 090603);广东省大学生创新项目(No 1057211018)
摘 要:目的观察巴戟天低聚糖(oligosaccharides of MorindaOfficinali,OMO)对Aβ25-35致拟痴呆模型大鼠学习记忆障碍的影响。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(0.125 mg.kg-1.d-1)组、OMO高剂量(60 mg.kg.d-1)组和OMO低剂量(20 mg.kg.d-1)组。连续灌胃给药25 d后,采用Morris水迷宫进行行为学检测;采用HPLC-ECD法检测脑组织中单胺类神经递质水平;采用HE染色后检测脑组织中海马CA1区锥体细胞和神经元数量,以及大脑皮质和前脑基底核神经元数量等指标。结果水迷宫实验结果显示,Aβ25-35模型组定位航行潜伏期明显长于空白组,其定位航行总路程明显高于空白组,而各给药组潜伏期明显缩短。空间探索实验结果显示,空白组大鼠在第一象限(即平台原所在区域)游泳时间(27.36±3.38 s)长于其他象限,差异具有统计学意义(P<0.05);与空白组比较,模型组在第一象限游泳时间(20.77±5.63 s)明显缩短,OMO高剂量组(31.93±3.39 s)比空白组延长,差异具有统计学意义(P<0.01),其余各组差异没有统计学意义(P>0.05)。与模型组比较,给药组在第一象限游泳时间明显延长,且差异具有统计学意义(P<0.01)。与模型组比较,各给药组单胺类神经递质水平升高;与模型组比较,各给药组海马CA1区椎体细胞和神经元数量增加,以及大脑皮质和前脑基底核神经元计数增多。结论实验结果显示OMO可以明显提高Aβ25-35致拟痴呆大鼠学习记忆能力,其机制可能与提高单胺类神经递质水平和抑制大脑神经元凋亡有关。Objective To assess effects of oligosaccharides from Morinda Officinalis on learning and memory dysfunction induced by β-amyloid in rats.Methods The dementia models of SD rats were prepared by injecting 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) group,blank group,sham operation group and the positive group(donepezil HCl,0.125 mg·kg^-1·d^-1) were designed at the same time.After 25 days' treatments,Morris water maze was used to test the behavior.And HPLC-ECD was used to measure the levels of monoamine neurotransmitter.Count the number of pyramidal neurons in hippocampus,neuron cells in hippocampal CA1,cerebral cortex and basal nucleus of Meynert after HE staining.Results The Morris water maze tests showed that the latency and total route of place navigation of model group were longer than blank group's,while the OMO treated groups were shorter.Spatial probe tests showed that the swimming time in the quadrant where the platform had been during the place navigation tests of blank group(27.36±3.38 s) was significantly longer(P0.01) than in other three quadrants.Compared with blank group,the model group's swimming time(20.77±5.63 s) in the first quadrant was significantly shortened(P0.01),while the OMO high-dose group(31.93±3.39 s) was significantly longer(P0.01),but the other groups' were not significant difference(P0.05).Compared with model group,the swimming time of all the treated groups were significantly longer.The levels of neurotransmitter were higher,and the number of pyramidal neurons in hippocampus,neuron cells in hippocampal CA1,cerebral cortex and basal nucleus of Meynert were obviously more of treated groups than those of model group.Conclusions The results show that the OMO can ameliorate the learning and memory dysfunction induced by β-amyloid in rats,and the mechanism may improve monoamines neurotransmitter levels and inhibit the brain neuron apoptosis.
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