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阿尔茨海默病大鼠     
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  alzheimer ' s disease rats
     Changes of Bcl-2 Protein Expression in the Frontal and Hippocampus Cells of Alzheimer's Disease Rats
     阿尔茨海默病大鼠海马额叶Bcl-2蛋白表达的改变
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     Study on relationship between effects of quercetin on learning and memory in Alzheimer's disease rats and apoptosis of hippocampus cells
     槲皮素对阿尔茨海默病大鼠学习记忆影响及与海马细胞凋亡关系的研究
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     Expression of MAPK in the hippocampus of Alzheimer' s disease rats model
     阿尔茨海默病大鼠模型海马MAPK的表达(英文)
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     Protective Effects of Dipfluzine on the Brain in Alzheimer's Disease Rats and Naturally Aged Rats
     双苯氟嗪对阿尔茨海默病大鼠及自然衰老大鼠的脑保护作用
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     Effect of Compound Danshen Tablets on amino acid neurotransmitters in brain of Alzheimer's disease rats
     复方丹参片对阿尔茨海默病大鼠脑内氨基酸类神经递质含量的影响
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  rats with alzheimer disease
     AIM:To observe the changes of postsynaptic protein ProSAP/Shank expression in the brain tissue of rat models, and investigate the neuroprotectice role of compound Jinsiwei in rats with Alzheimer disease.
     目的:观察突触后蛋白ProSAP/Shank在模型大鼠脑内表达的变化,探讨复方金思维对阿尔茨海默病大鼠的神经保护作用。
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     OBJECTIVE:To observe whether acidic peptide can inhibit the production of N-methyl-D-aspartate receptor(NMDAR)and beta-amyloid(β-amyloid)in brain,and accelerate the production and excretion of nerve growth factor(NGF)in rats with Alzheimer disease.
     目的:观察酸性肽能否抑制阿尔茨海默病大鼠脑内N-甲基-D-天冬氨酸受体和淀粉样β蛋白的产生以及促进神经生长因子的产生和分泌。
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     Effects of compound Jinsiwei on expression of ProSAP/Shank protein in brain tissue of rats with Alzheimer disease
     复方金思维对阿尔茨海默病大鼠脑组织ProSAP/Shank蛋白表达的影响
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     Effect of learning and memory training on spatial cognitive ability in rats with Alzheimer disease and its protective effect for brain tissue
     学习记忆训练对阿尔茨海默病大鼠空间认知能力及脑组织的保护作用
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     Effects of fufang jinsiwei versus placebo,saline and Aricept on the expression of protein 95 in post-synapse dense area of brain tissue in rats with Alzheimer disease
     复方金思维对阿尔茨海默病大鼠脑组织突触后致密区蛋白95表达的影响与安慰剂及盐酸多奈哌齐干预效果的比较
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  alzheimer ' s rat
     The Study about Expression Changes of MAPK and NMDAR in the Hippocampus of Alzheimer's Rat
     阿尔茨海默病大鼠海马MAPK和NMDAR表达变化的研究
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     An Simple Alzheimer's Rat Model Induced by Okadaic Acid
     一种简易的实验性阿尔茨海默病大鼠模型
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  rats with alzheimer ' s disease
     Changes of PKC and GDNF in hippocampus of rats with Alzheimer's disease
     阿尔茨海默病大鼠海马PKC和GDNF的变化
短句来源
     Effects of fetal rat neural stem cells (NSCs) transplantation on expression of GFAP and S-100β in hippocampus of rats with Alzheimer's disease
     胎鼠神经干细胞移植对阿尔茨海默病大鼠海马区的GFAP与S-100β表达的影响
短句来源
     Changes of extracellular regulated protein kinase in rats with Alzheimer's disease
     阿尔茨海默病大鼠海马细胞外调节蛋白激酶的变化
短句来源
     Effect of Yuanzhi on Learning and memory and AchE Activity of Model Rats with Alzheimer's disease
     中药远志对阿尔茨海默病大鼠模型学习记忆和胆碱酯酶活性的影响
短句来源
     Effect of Jiannao Yizhi decoction on learning memory and oxidative stress in rats with Alzheimer's disease
     健脑益智汤对阿尔茨海默病大鼠学习记忆和氧化应激的影响
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The protective effect of Bushen Yizhi Decoction(BYD)on brain cholinergic system in rat model with Alzheimer's disease(AD)was studied with histochemical technique to visualize acetylcholinesterase.AD rat model was established by intraperitoneral injection of D-galactose and ibotenic acid injection into bilateral Meynert nucles.The results showed that the density of acetylcholinesterase_containing fibers in extensive region of model rat brain treated with gastric perfusion of BYD was higher than that in model...

The protective effect of Bushen Yizhi Decoction(BYD)on brain cholinergic system in rat model with Alzheimer's disease(AD)was studied with histochemical technique to visualize acetylcholinesterase.AD rat model was established by intraperitoneral injection of D-galactose and ibotenic acid injection into bilateral Meynert nucles.The results showed that the density of acetylcholinesterase_containing fibers in extensive region of model rat brain treated with gastric perfusion of BYD was higher than that in model rat brain.This indicates BYD exerts a certain protective effect on brain cholinergic neuron in rat model with AD.

为探讨自制方补肾益智方 (由蛇床子、枸杞子、女贞子、人参、制首乌等组成 )治疗阿尔茨海默病(Alzheimerdisease ,AD)的可能神经生物学机制 ,应用乙酰胆碱酯酶组织化学染色方法 ,研究了该方对D -半乳糖合并鹅膏蕈氨酸损毁大脑Meynert基底核的实验性阿尔茨海默病大鼠模型脑内胆碱能神经系统的保护作用 ,结果显示 :补肾益智方灌胃组大鼠脑内广泛区域的乙酰胆碱酯酶阳性神经纤维密度较模型对照组增加 (P <0 .0 5或P <0 .0 1) ,提示该方对AD模型脑内胆碱能神经元具有一定的保护作用。

Objective To observe the effects of saponins of Panax notoginseng (PNS) on the brain energy metabolism and mitochondrial respiratory function of oxidative damaged rat model mimic to Alzheimer disease (AD). Methods Oxidative damaged rat model mimic AD (AD group) was established by injection of dihydroxy fumaric acid (DHF) and FeCl3 ADP into the left lateral ventricle of rats. The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and phosphate creatine...

Objective To observe the effects of saponins of Panax notoginseng (PNS) on the brain energy metabolism and mitochondrial respiratory function of oxidative damaged rat model mimic to Alzheimer disease (AD). Methods Oxidative damaged rat model mimic AD (AD group) was established by injection of dihydroxy fumaric acid (DHF) and FeCl3 ADP into the left lateral ventricle of rats. The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and phosphate creatine (Pcr) in brain were determined by high performance liquid chromatography (HPLC). The mitochondrial functions (R3, R4, P/O, and OPR) were observed by Clark oxygen electrode method. The difference in the above parameters in rats in the control group (injection of saline), model group, and administration group (injection of PNS) was observed. Results The levels of ATP, Pcr, and R3, R4, P/O, and OPR of rats in AD group were significantly lower than those in the control group (0.9% NaCl instead of DHF FeCl3 ADP), but those in PNS group were higher than those in the AD group. Conclusion PNS can improve brain energy metabolism and mitochondrial function of oxidative damaged rats, suggesting that PNS could be used for the treatment of AD.

目的 探讨三七皂甙对氧化损伤型类阿尔茨海默病大鼠脑组织能量代谢的影响。方法 采用二羟延胡索酸 (DHF)和FeCl3 ADP左侧脑室注射法制作大鼠氧化损伤型类AD大鼠模型 ;用高效液相法测定脑组织中含高能磷酸键的ATP、磷酸肌酸等的含量 ,用氧电极法测量线粒体呼吸链呼吸功能 ,观察分析各指标在同样插管但注射生理盐水的手术对照组以及模型组、给药组 (给三七皂甙 )之间的差异。结果 给药组ATP、磷酸肌酸显著高于模型组 ,但仍低于对照组 ,给药组ADP、AMP显著低于模型组。给药组线粒体 3、4态呼吸以及P/O显著高于模型组。结论 三七皂甙可以有效地改善氧化损伤型类AD大鼠脑能量代谢及线粒体功能 ,提示其可用于AD的治疗。

AIM:To establish rat models of non-hereditary Alzheimer's disease(AD) by dama ging bilateral nucleus basalis of Meynert(NBM) with quinolinic acid. METHODS:Bilateral NBM of elderly rats were damaged with quinolinic acid(150 nm ol in 2 μL for each NBM).One-off step-down passive avoidance training and wat er-maze spatial localization task were conducted to observe the ability of lear ning and memory in the rats .The effects of 1,2,3,4-tetrahydroacridine(THA)on learning and memory of the rat with damaged NBM were...

AIM:To establish rat models of non-hereditary Alzheimer's disease(AD) by dama ging bilateral nucleus basalis of Meynert(NBM) with quinolinic acid. METHODS:Bilateral NBM of elderly rats were damaged with quinolinic acid(150 nm ol in 2 μL for each NBM).One-off step-down passive avoidance training and wat er-maze spatial localization task were conducted to observe the ability of lear ning and memory in the rats .The effects of 1,2,3,4-tetrahydroacridine(THA)on learning and memory of the rat with damaged NBM were also observed. RESULTS:Compared with the sham-lesion group,the number of errors in the step -down trial 13 days after NBM damage was increased significantly(in the learnin g test,1.25±0.71 vs 3.75±1.28,q=6.83,P< 0.01;in the retest, 0.50±0.53 vs 2.00 ±0.76,q=7.42,P< 0.001). So was the training times to reach the criterion in the water-maze task 16 days after damage(q= 22.16,P< 0.001).Compared with the qui nolinic acid group, the number of errors in the step-down trial after the rats were intraperitoneally injected with THA 10 mg/(kg·d ) for 13 days was decrease d obviously(P< 0.01) .So was the training times to reach the criterion in the wa ter maze task 16 days after intraperitoneal injection of THA(q= 20.38,P< 0.01). CONCLUSION: Rat models of non-hereditary AD can be made by damaging bilateral NBM with quinolinic acid.

目的:应用喹啉酸损毁Meynert基底核建立非遗传性阿尔茨海默病大鼠模型。方法:应用喹啉酸(每侧150nmol,2μL)损毁老年大鼠双侧Meynert基底核,一次性训练被动回避跳台实验和水迷宫空间分辨能力测试,研究大鼠学习记忆的改变,并观察1,2,3,4四氢吖啶(THA)对Meynert基底核损毁大鼠学习记忆的改善作用。结果:与假损伤组相比,喹啉酸损伤Meynert基底核后13d,大鼠在跳台中出现的错误反应次数明显增多,学习中为(1.25±0.71)次比(3.75±1.28)次(q=6.83,P<0.01),重测验中为(0.50±0.53)次比(2.00±0.76)次(q=7.42,P<0.001)。损伤后16d,大鼠学会迷宫所需的训练次数显著增加(q=22.16,P<0.001)。与喹啉酸组对比,腹腔注射THA10mg/(kg·d)13d后,Meynert基底核损伤后大鼠在跳台中出现的错误反应次数明显减少(P<0.01),腹腔注射THA16d后学会迷宫所需的训练次数也显著减少(q=20.38,P<0.01)。结论:喹啉酸损毁老年大鼠双侧Meynert基底核,能够建立非遗传性阿尔茨海默病大鼠...

目的:应用喹啉酸损毁Meynert基底核建立非遗传性阿尔茨海默病大鼠模型。方法:应用喹啉酸(每侧150nmol,2μL)损毁老年大鼠双侧Meynert基底核,一次性训练被动回避跳台实验和水迷宫空间分辨能力测试,研究大鼠学习记忆的改变,并观察1,2,3,4四氢吖啶(THA)对Meynert基底核损毁大鼠学习记忆的改善作用。结果:与假损伤组相比,喹啉酸损伤Meynert基底核后13d,大鼠在跳台中出现的错误反应次数明显增多,学习中为(1.25±0.71)次比(3.75±1.28)次(q=6.83,P<0.01),重测验中为(0.50±0.53)次比(2.00±0.76)次(q=7.42,P<0.001)。损伤后16d,大鼠学会迷宫所需的训练次数显著增加(q=22.16,P<0.001)。与喹啉酸组对比,腹腔注射THA10mg/(kg·d)13d后,Meynert基底核损伤后大鼠在跳台中出现的错误反应次数明显减少(P<0.01),腹腔注射THA16d后学会迷宫所需的训练次数也显著减少(q=20.38,P<0.01)。结论:喹啉酸损毁老年大鼠双侧Meynert基底核,能够建立非遗传性阿尔茨海默病大鼠模型。目的:应用喹啉酸损毁Meynert基底核建立非遗传性阿尔茨海默病大鼠模型。方法:应用喹啉酸(每侧150nmol,2μL)损毁老年大鼠双侧Meynert基底核,一次性训练被动回避跳台实验和水迷宫空间分辨能力测试,研究大鼠学习记忆的改变,并观察1,2,3,4四氢吖啶(THA)对Me

 
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