Preventive Effects of Rhodosin and Melatonin from Damage Induced by β-Amyloid1-40 in Senile Rats

Objective: To study the protective and therapeutic effects of Rhodosin and Melatonin on Alzheimers disease(AD) rats. Methods: D-galactose was intraperitoneally injected in rats for 6 weeks and β-Amyloid1-40(Aβ1-40) was injected into bilateral hippocampus to make AD models. Rhodosin and Melatonin were intraperitoneally injected in rats for 4 weeks to determine the protective and therapeutic effects on rats with AD. Y-maze test, and passive avoidance task were used to determine the ability of learning and memory. The content of lipofuscin in the central cortex, the viscous coefficient of mitochondrial membrane, the activity of superoxide dismutase and the content of malondialdehyde in both sides of hippocampus were determined. And the apoptosis of hippocampus neurons was determined with transmission electron microscopy(TEM). Results: Melatonin as an antioxidant significantly improved learning and memory deficits in the rats with AD and reduced the increase in SOD, MDA, the viscous coefficient and lipofuscin to their normal levels, and it also showed the protective effects of apoptosis. Rhodosin showed the similar effects. Conclusion: Rhodosin and Melatonin had preventive and therapeutic effects on rats with AD probably by affecting the free radical levels in rats.     

Altered angiotensin-converting enzyme and its effects on the brain in a rat model of Alzheimer disease

Background Alzheimer disease （AD） is a neurodegenerative disease related to aging. At present, its pathological mechanisms remain unclear. Family members of the renin-angiotensin system （RAS） play a role in neuronal plasticity, as well as formation of learning and memory. In this study, we explore the effects of altered angiotensin-converting enzyme （ACE）, and investigate the possible mechanisms of perindopril, an ACE inhibitor, on brain structure and function in a rat model of AD, as well as the role that ACE plays in AD. Methods Sixty Sprague-Dawley rats were selected and randomly divided into 3 groups： control, AD, and perindopril. Each group consisted of 20 rats, with 10 rats for determining pathology, and the remaining 10 rats for quantifying ACE activity. The rat AD model was established by stereotactically injecting amyloid beta protein （A-beta） 1-42 into the right hippocampus. Learning and memory functions were tested using the Y-type electric maze. The number and morphology of abnormal neurons were determined by haematoxylin and eosin staining. Amyloid deposition was measured by Congo red staining. Finally, ACE activity was estimated by spectrophotometry. Results Compared with the control group, the number of times needed to escape electrical stimuli increased （23.70±3.13, P 〈0.001）, the number of normal neurons in the CA1 region was reduced （density of 96.5±32.6/mm, P 〈0.001）, amyloid deposition was obvious, and ACE activity increased （（34.4±6.6） nmol.g-1.min-1, P 〈0.001） in the AD group. In the perindopril group, the number of times needed to escape electrical stimuli decreased （18.50±3.66, P 〈0.001）, the number of abnormal neurons increased （density of CA1 neurons was 180.8±28.5/mm, P 〈0.001）, amyloid deposition was reduced, and ACE activity was down-regulated （（26.2±6.2） nmol.g-1.min-1, P 〈0.001）. Conclusions ACE activity increased in the brains of AD rats. Perindopril improved learning and memory in AD rats, which correlated with de     

Bone Marrow-Derived Mesenchymal Stem Cells Incubated with Tanshinone IIA Aattenuates Learning and Memory Impairment Induced by β-amyloid and its Underlying Mechanisms in Rats

Objective：The present study was designed to investigate the neuroprotective effect of mesenchymal stem cells （MSC） which incubated with tanshinone IIA on β-amyloid （Aβ）-induced learning and memory impairment in rats,and further explore the underlying potential mechanisms. Methods：60 healthy male SD rats were randomly divided into 4 groups：sham-operated group,model group,MSC group,MSC+tanshinone group IIA（ n=15）.The rats of model group were injected into the hippocampal with aggregation of 5 μL Aβ25-35（ 2 μg·μL-1） to establish the model of learning and memory impairment. 1 week after surgery,the MSC were injected into the hippocampus,while the rats of model group were injected with volume-matched DMEM,instead. 2 weeks after surgery, Morris water maze （MWM） test was applied to evaluate spatial learning and memory ability of rats,then the rats were sacrifi ced. The survival status of hippocampal neurons was detected by HE and Tunel staining;the formation of hippocampal senile plaques was detected by thiofl avin S staining;the protein expression of Aβ1-42,p-Tau and AMPK in mouse hippocampus were detected by Western blot,respectively;the expression of AMPK mRNA was detected by PCR and the activity of SOD,T-AOC,GSH-PX and content of MDA in plasma by the kits.Results：Compared with sham-operated group, the mean escape latency was markedly increased and the time percentage in target quadrant showed notable decrease in model group;large number of the formation of senile plaque in the hippocampus was detected;the number of surviving neurons in hippocampus was signifi cantly decreased and the apoptosis increased;the protein expression of Aβ1-42 and p-Tau were increased;the mRNA expression and protein levels of AMPK was decreased;the activity of SOD,T-AOC,GSH-PX were decreased and content of MDA increased in plasma.However,compared with model group,the escape latency of MSC group and MSC+Tanshinone group rats was shorter,time percentage in the target quadrant and target quadrant frequency were markedly increased;moreover,the formation of senile plaque in the hippocampus was decreased;the number of surviving neurons in hippocampus was signifi cantly increased;the protein expression of Aβ1-42 and p-Tau were decreased;the mRNA expression and protein levels of AMPK was increased;the activity of SOD,T-AOC,GSH-PX were increased and content of MDA decreased in plasma.And MSC+tanshinone group was more significant than the
MSC group. Conclusion：Under the experimental conditions,MSC incubated with tanshinone ⅡA signifi cantly ameliorates spatial learning and memory impairment and reduce Aβ aggregation and tau protein phosphorylation levels induced by Aβ25-35 in rats,and its potential mechanism may be related
toanti-oxidative stress.     

The Influences of Electroacupuncture on the Quantitative Changes of Ultra Structure in CA3 Sector of the Hippocampus of VD Rats

Objective To observe the effect of electroacupuncture （EA） on learning and memory and the pathology morphologic of nerve and the quantitative changes of synapses in CA3 sector of the hippocampus on vascular dementia （VD） rats. Methods The VD rats were modeled with method of global ischemia reperfusion by 4 vascular occlusion （4-vo）. Morris water maze tests were used for a behavioral study. The changes of the ultra structure parameter in CA3 sector of the hippocampus were studied with transmission electron microscope and picture analysis system. Results The model group animals needed more escape time than the control group, and they did not swim longer in platform quadrant than in the others in the Morris water tests. In the control group and electro-acupuncture group, the modality configuration of cells in CA3 sector of the hippocampus was normal, and the normal and abnormal chromatin was obvious. The configuration of endoplasmic reticulum, chondriosome and synapses was normal. The front and back membrane of the synapses was clear. In the VD group, the cells were atrophied and dwindled. The front and back membrane of the synapses was illegible. The clearance, PSD and interphase curvature on area of Gray type Ⅰ synapses in CA3 sector of the hippocampus in VD rats were decreased significantly. In the EA group, the animals cut the escape time mostly and they swam more times in platform quadrant than in other three quadrants. The interphase curvature, cleft and PSD on area of Gray type Ⅰ synapses in CA3 sector of the hippocampus were increased significantly. Conclusion EA can improve learning and memory of VD rats by restraining the disappearance of nerve cells, and influencing the structure parameter of synapses in CA3 sector of the hippocampus.     

Huannao Yicong Decoction(还脑益聪方) Extract Reduces Inflammation and Cell Apoptosis in Aβ_(1-42)-Induced Alzheimer's Disease Model of Rats

Objective: Huannao Yicong Decoction(还脑益聪方, HYD), an effective herbal formula against Alzheimer's disease(AD), has been proven to have neuroprotective action in amyloid β-protein_(1-42))(Aβ_(1-42))-induced rat model. This study was designed to characterize mechanisms by which HYD leads to suppression of inflammation and apoptosis in the brains of Aβ_(1-42)-induced rat. Methods: A total of 72 rats were divided into 6 groups, which were referred to as: sham operation group, model group, donepezil-treated group, HYD low-dose group(HYDL), HYD middle-dose group(HYDM) and HYD high-dose group(HYDH). Rats in HYDL, HYDM and HYDH were injected with Aβ_(1-42) at the CA1 region of hippocampus to form AD model and were fed the HYD extract at different dose of 3.78, 7.56 and 18.90 g crude drug/kg. The behavioral changes of rats were evaluated by Morris water maze(MWM) before sacrifice. Pathological changes of the brain tissue were evaluated using hematoxylin eosin(HE) staining. The levels of interleukin-1(IL-1) and tumor necrosis factor-α(TNF-α) were measured by radioimmunoassay. The levels of Aβ and proteins that are associated with apoptosis such as B-cell lymphoma-2 protein(Bcl-2), Bcl-2-associated X protein(Bax), cysteine-aspartic protease(caspase)-3,-8,-9 and-12 in serum were measured by immunohistochemistry. Results: Compared with the sham operation group, the spatial learning and memory abilities of AD rats were significantly decreased(P0.05 or P0.01; Expressions of IL-1, TNF-α, Aβ and apoptosis-signaling proteins caspase-3,-8,-9,-12 were significantly up-regulated(P0.05 or P0.01). The ratio of Bcl-2 to Bax were significantly decreased in the model group(P0.01). When treated with HYD extract, the spatial learning and memory abilities of AD-model rats were significantly increased(P0.05 or P0.01), IL-1, TNF-α, Aβ, caspase-3,-8,-9 and-12 were down-regulated(P0.05 or P0.01), and the ratio of Bcl-2 to Bax were reduced(P0.05 or P0.01). Conclusions: HYD extract can improve the learning and memory ability deficits, alleviate the inflammatory response and pathological manifestations induced by Aβ_(1-42) injection in the rat model of AD. HYD down-regulates the levels of IL-1, TNF-α and Aβ, and decreases the rate of apoptosis by modulating apoptosis-signaling-related proteins such as caspase-3,-8,-9, and-12.     

Huannao Yicong Decoction (还脑益聪方) extract reduces inflammation and cell apoptosis in Aβ1-42-induced Alzheimer's disease model of rats

Objective: Huannao Yicong Decoction (还脑益聪方, HYD), an effective herbal formula against Alzheimer''s disease (AD), has been proven to have neuroprotective action in amyloid β-protein1-42 (Aβ1-42)-induced rat model. This study was designed to characterize mechanisms by which HYD leads to suppression of inflammation and apoptosis in the brains of Aβ1-42-induced rat. Methods: A total of 72 rats were divided into 6 groups, which were referred to as: sham operation group, model group, donepezil-treated group, HYD low-dose group (HYDL), HYD middle-dose group (HYDM) and HYD high-dose group (HYDH). Rats in HYDL, HYDM and HYDH were injected with Aβ1-42 at the CA1 region of hippocampus to form AD model and were fed the HYD extract at different dose of 3.78, 7.56 and 18.90 g crude drug/kg. The behavioral changes of rats were evaluated by Morris water maze (MWM) before sacrifice. Pathological changes of the brain tissue were evaluated using hematoxylin eosin (HE) staining. The levels of interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) were measured by radioimmunoassay. The levels of Aβ and proteins that are associated with apoptosis such as B-cell lymphoma-2 protein (Bcl-2), Bcl-2-associated X protein (Bax), cysteine-aspartic protease (caspase)-3, -8, -9 and -12 in serum were measured by immunohistochemistry. Results: Compared with the sham operation group, the spatial learning and memory abilities of AD rats were significantly decreased (P<0.05 or P<0.01; Expressions of IL-1, TNF-α, Aβ and apoptosis-signaling proteins caspase-3, -8, -9, -12 were significantly up-regulated (P<0.05 or P<0.01). The ratio of Bcl-2 to Bax were significantly decreased in the model group (P<0.01). When treated with HYD extract, the spatial learning and memory abilities of AD-model rats were significantly increased (P<0.05 or P<0.01), IL-1, TNF-α, Aβ, caspase-3, -8, -9 and -12 were down-regulated (P<0.05 or P<0.01), and the ratio of Bcl-2 to Bax were reduced (P<0.05 or P<0.01). Conclusions: HYD extract can improve the learning and memory ability deficits, alleviate the inflammatory response and pathological manifestations induced by Aβ1-42 injection in the rat model of AD. HYD down-regulates the levels of IL-1, TNF-α and Aβ, and decreases the rate of apoptosis by modulating apoptosis-signaling-related proteins such as caspase-3, -8, -9, and -12.     

Effect of behavior training on learning,memory and the expression of NR2B,GluR1 in hippocampus of rats offspring with fetal growth restriction

Objective： To study effects of behavior training on learning, memory and the expression of NR2B, GluR1 in hippocampus of rat＇ s offspring with fetal growth restriction（FGR）. Methods： The rat model of FGR was established by passive smoking method. The rats offspring were divided into the FGR group and the control group, then randomly divided into the trained and untrained group, respectively. Morris water maze test was proceeded on postnatal month（PM2/4） as a behavior training method, then the learning-memory of rats was detected through dark-avoidance and step-down tests. The expressions of NR2B and GluR1 subunits in hippocampal CA1 and CA3 areas were detected by immunohistochemical method. Results： In the dark-avoidance and step-down tests, the performance record of rats with FGR was worse than that of control rats, and the behavior-trained rats was better than the untrained rats, when the FGR model and training factors were analyzed singly. The model factor and training factor had significant interaction（P 〈 0.05）. The expressions of NR2B and GluR1 subunits in hippocampal CA1 and CA3 areas of rats with FGR reduced. In contrast, the expressions of GluR1 and NR2B subunits in CA1 area of behavior-trained rats increased, when the FGR model and training factors were analyzed singly. Conclusion： These findings suggested that the effect of behavior training on the expressions of NR2B and GluR1 subunits in CA1 area should be the mechanistic basis for the training-induced improvement in learning-memory abilities.     

Effect of behavior training on learning,memory and the expression of NR2B,GluR1 in hippocampus of rats offspring with fetal growth restriction

Objective:To study effects of behavior training on learning,memory and the expression of NR2B,GluR1 in hippocampus of rat's offspring with fetal growth restriction(FGR).Methods:The rat model of FGR was established by passive smoking method.The rats offspring were divided into the FGR group and the control group,then randomly divided into the trained and untrained group,respectively. Morris water maze test was proceeded on postnatal month(PM2/4)as a behavior training method,then the learning-memory of rats was detected through dark-avoidance and step-down tests.The expressions of NR2B and GluR1 subunits in hippocampal CA1 and CA3 areas were detected by immunohistochemical method.Results:In the dark-avoidance and step-down tests,the performance record of rats with FGR was worse than that of control rats,and the behavior-trained rats was better than the untrained rats,when the FGR model and training factors were analyzed singly.The model factor and training factor had significant interaction(P<0.05).The expressions of NR2B and GluR1 subunits in hippocampal CA1 and CA3 areas of rats with FGR reduced.In contrast,the expressions of GluR1 and NR2B subunits in CA1 area of behavior-trained rats increased,when the FGR model and training factors were analyzed singly. Conclusion:These findings suggested that the effect of behavior training on the expressions of NR2B and GluR1 subunits in CA1 area should be the mechanistic basis for the training-induced improvement in learning-memory abilities.     

β-淀粉样蛋白致大鼠Alzheimer病模型的研究

目的 :模拟人类Alzheimer病 (AD)的大鼠病理模型 ,观察其学习记忆及病理性改变。方法 :大鼠双侧海马微量注射聚合态Aβ1 40 制备AD动物模型 ,Y 型迷宫测定大鼠学习记忆能力 ,HE染色、刚果红染色和银染检测病理变化。结果 :海马内注射Aβ1 40 可引起大鼠学习记忆能力下降 ,注射区Aβ沉积 ,神经元丢失及胶质细胞增生 ,神经原纤维缠结。结论 :Aβ1 40 海马内注射能较好的模拟AD的学习记忆障碍、神经元损伤等行为学和病理学等方面的特征 ,作为AD研究较好的动物模型。     

何首乌对Aβ1-40诱导的大鼠海马神经元内BDNF表达的影响

目的：探讨Aβ1-40对海马CA1区神经元脑源性神经营养因子（brain—derived neurotrophic factor，BONY）表达的影响，以及何首乌对其的干预作用。方法：右侧海马微量注射Aβ1-40，观察海马BDNF的表达变化；并使用何首乌浸膏对大鼠模型进行干预治疗。动物存活30d后，用“Y”迷宫检测各组动物学习和记忆能力；采用免疫组织化学方法和Westem-blot检测海马CA1区神经元BDNF的表达；应用尼氏染色法观察海马CA1区神经元数目和形态。结果：Aβ1—40能够导致大鼠学会躲避电刺激所需的“尝试次数”明显增加；BDNF蛋白的表达明显下降，并可以在海马观察到Aβ1-40的沉积；CA1区的神经元出现胞体肿胀、排列散乱等形态改变，且使用何首乌对动物模型干预治疗30d后。大鼠的躲避电刺激所需的“尝试次数”明显下降；海马CA1区神经元BDNF表达明显上调。结论：使用Aβ1—40在体内能够下调海马CA1区神经元BDNF表达。何首乌干预治疗30d，能够改善动物的学习和记忆能力，并能减少Aβ1-40对海马CA1区神经元BDNF表达的抑制作用。     

银杏内酯和胰岛素对拟AD模型大鼠学习记忆的影响

目的：建立拟AD大鼠模型，研究银杏内酯和胰岛素对拟AD模型大鼠学习记忆的影响。方法：采用冈田酸（OA）海马CA1区微量注射建立拟AD大鼠模型，分为银杏内酯组，胰岛素组。银杏内酯组腹腔注射银杏内酯，胰岛素组侧脑室微量注射速效基因合成人胰岛素，分别设对照组。冈田酸末次注射2周后水迷宫行为学试验检测其学习记忆，Bielschowsky染色观察海马CA1区老年斑（SP）和神经原纤维缠结（NFT）。结果：拟AD模型组定向航行试验于第2天开始平均逃避潜伏期与对照组比较明显延长（P〈0．05或P〈0．01），空间探索试验原站台象限活动时间明显缩短（P〈0．01）；与拟AD模型组比较，银杏内酯组及胰岛素组平均逃避潜伏期明显缩短（P〈0．05或P〈0．01），原站台象限活动时间明显延长（P〈0．01）。Bielschowsky染色观察对照组大鼠海马CA1区未见明显改变，拟AD模型组大鼠海马CA1区形成NFT，细胞外有SP；银杏内酯组和胰岛素组大鼠海马CA1区少见或未见SP或NFT。结论：银杏内酯腹腔注射或胰岛素微量侧脑室注射均可减少拟AD模型大鼠海马CA1区SP和NFT的形成，减轻OA对大鼠海马的病理损害，显著改善拟AD模型大鼠学习记忆功能。     

丁苯酞对AD大鼠模型认知及海马Aβ、NR2b表达的影响

目的观察丁苯酞对AD大鼠模型的学习记忆能力及海马Aβ、NR2b表达的影响。方法采用大鼠海马立体定向注射凝聚态Aβ1-40诱导AD模型。采用Morris水迷宫评价大鼠学习记忆能力,采用免疫组织化学染色法测定海马区Aβ、NR2b蛋白的表达。结果丁苯酞低剂量组和高剂量组能明显减少海马Aβ的沉积,有效促进海马CA1区NR2b的表达（P〈0.01）;对AD大鼠模型的学习、空间记忆能力有明显的改善（P〈0.01）;而高剂量组和低剂量组对AD大鼠模型的改善作用没有明显差异。结论 AD大鼠模型学习记忆的改变与海马Aβ、NR2b变化相关,丁苯酞可能通过减少海马Aβ的沉积、促进CA1区NR2b的表达从而改善AD大鼠模型的学习和空间记忆能力。     

Suppressive effects of melatonin on amyloid-beta-induced glial activation in rat hippocampus

BACKGROUND: Growing evidence indicates that activated glia, as a result of chronic inflammation, are associated with amyloid-beta peptide (Abeta) deposits in the brain of Alzheimer's disease (AD) patients. The purpose of the present study was to investigate, in vivo, the effects of melatonin on glia activation, which may contribute to improved learning and memory in amnesic rats induced by amyloid-beta peptide 25-35 (Abeta25-35). METHODS: We examined cognitive function using the Morris water maze test. Expression of interleukin 1alpha (IL-1alpha) or complement 1q (C1q) in rat hippocampal tissue was determined by immunohistochemistry. RESULTS: It was found that Abeta25-35 injected into rat hippocampus induced an impairment in learning and memory and a marked increase of positive glial cells expressing IL-1alpha and C1q in hippocampus, compared with the controls. This suggests that glial activation triggered by Abeta25-35 parallels the dysfunction of learning and memory. Melatonin, at doses of 0.01, 0.1, and 1 mg/kg (i.g. for 10 days), improved learning and memory of rats treated with Abeta25-35. Cells expressing IL-1alpha and C1q were significantly decreased in hippocampus by pretreatment with melatonin at doses of 0.1 mg/kg and 1 mg/kg, but not at the dose of 0.01 mg/kg. CONCLUSIONS: Our data indicate that melatonin inhibited expressions of proinflammatory factors, which may contribute to improvement of learning and memory function in AD.     

p38MAPK在Aβ25-35诱导AD大鼠海马CA1区表达的研究

OBJECTIVE: To investigate the changes of p38MAPK expression in a rat model of Alzheimer disease (AD). METHODS: Seventy-two adult SD rats were randomized equally into 4 groups, and a single-dose injection of Abeta(25-35) (dementia group), normal saline (saline group), SB203580 (inhibitor group), or DMSO (inhibitor control group) was administered into the lateral cerebral ventricle. Y-maze tast was performed to evaluate the behavioral changes of the rats after the injections, and on days 4, 7 and 14 after the injection, p38MAPK expression in the hippocampal CA1 area was measured by means of immunohistochemistry. RESULTS: On days 7 and 14 following Abeta(25-35) injection, the training times, error number and total reaction time were significantly higher in dementia group than in saline group (P<0.05), but all these indices were significantly lowered in the inhibitor group as compared with the dementia group (P<0.05). Immunohistochemistry revealed obvious p38 expression in the dementia group 4 days after Abeta(25-35) injection, which increased significantly with the passage of time (P<0.01). The gray scale in the inhibitor group was significantly higher than that in the dementia group (P<0.01). CONCLUSION: p38MAPK activation in the hippocampal CA1 area is an event that persists during the entire course of Abeta(25-35)-induced AD in rats, and the inhibitor SB203580 prevents p38MAPK expression and improves the learning and memory abilities of the rats.     

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

目的 观察槲皮素(Que)对阿尔茨海默病(Alzheimer’s desease，AD)模型大鼠学习记忆影响并探讨其与海马细胞凋亡的关系。方法 用立体定位技术对海马CA1区微量注射喹啉酸(QA)造成AD模型；Y形迷宫检测大鼠学习记忆水平；电子显微镜、流式细胞仪检测海马细胞凋亡。结果 Que可明显提高QA所致痴呆大鼠学习记忆水平，显著降低海马细胞凋亡率。结论 Que对AD大鼠的保护作用与降低海马细胞凋亡率有关。     

蛇床子素减轻Aβ（25-35）诱导的大鼠学习记忆减退及海马神经元结构损伤

目的观察蛇床子素对-淀粉样蛋白25-35片段（Aβ25-35）诱导的大鼠学习记忆减退及海马神经元结构损伤的影响。方法 40只雄性SD大鼠随机均分为假手术组、模型组、阳性药组及蛇床子素组,阳性药组每日1次灌胃多奈哌齐1 mg/kg,蛇床子素组每日1次灌胃蛇床子素40 mg/kg,连续17 d,假手术组、模型组灌胃等体积的生理盐水,3 d后右侧脑室注射Aβ25-35制模,制模后d 10开始Morris水迷宫检测大鼠的空间记忆能力,透射电镜观察大鼠海马CA1区神经元结构损伤。结果右侧脑室注射Aβ25-35后,大鼠在定向航行实验中的逃避潜伏期明显增加（〈0.01）,空间探索实验中的校正逃避潜伏期缩短（〈0.01）,海马CA1区神经元结构明显受损;然而,蛇床子素及多奈哌齐明显缩短了大鼠的定向航行实验中的逃避潜伏期（〈0.01）,延长了空间探索实验中的校正逃避潜伏期（〈0.01）,减轻了海马CA1区神经元结构损伤。结论蛇床子素可减轻Aβ25-35诱导的大鼠学习记忆减退及海马神经元结构损伤。     

替勃龙对阿尔茨海默病模型大鼠的学习记忆能力及神经元凋亡的影响

目的观察替勃龙（tibolone）对AD大鼠的学习记忆能力及神经元凋亡的影响。方法用立体定位技术对海马CA1区微量注射Aβ建立AD模型;Morris水迷宫检测大鼠记忆水平;TUNEL染色法检测海马凋亡。结果替勃龙可明显提高Aβ所致痴呆大鼠学习记忆水平,显著降低海马细胞凋亡率。结论替勃龙对AD大鼠的保护作用与降低海马细胞凋亡率有关。