检索结果-南通市图书馆

Enhancement of oligodendrocyte autophagy alleviates white matter injury and cognitive impairment induced by chronic cerebral hypoperfusion in rats

引用

Acta Pharmaceutica Sinica B 2023年第5期13卷 2107-2123页

作者： Huiyang Wang Yueyang Liu Zhenkun Guo Minghui Cui Peng Pang Jingyu Yang Chunfu Wu Department of Pharmacology Shenyang Pharmaceutical UniversityShenyang 110016China

Cognitive impairment caused by chronic cerebral hypoperfusion(CCH)is associated with white matter injury(WMI),possibly through the alteration of autophagy.Here,the autophagy—lysosomal pathway(ALP)dysfunction in white matter(WM)and its relationship with cognitive impairment were investigated in rats subjected to two vessel occlusion(2VO).The results showed that cognitive impairment occurred by the 28th day after 2VO.Injury and autophagy activation of mature oligodendrocytes and neuronal axons sequentially occurred in WM by the 3rd day.By the 14th day,abnormal accumulation of autophagy substrate,lysosomal dysfunction,and the activation of mechanistic target of rapamycin(MTOR)pathway were observed in WM,paralleled with mature oligodendrocyte death.This indicates autophagy activation was followed by ALP dysfunction caused by autophagy inhibition or lysosomal dysfunction.To target the ALP dysfunction,enhanced autophagy by systemic rapamycin treatment or overexpression of Beclin1(BECN1)in oligodendrocytes reduced mature oligodendrocyte death,and subsequently alleviated the WMI and cognitive impairment after CCH.These results reveal that early autophagy activation was followed by ALP dysfunction in WM after 2VO,which was associated with the aggravation of WMI and cognitive impairment.This study highlights that alleviating ALP dysfunction by enhancing oligodendrocyte autophagy has benefits for cognitive recovery after CCH.

关键词： chronic cerebral hypoperfusion Two vessel occlusion White matter Cognitive impairment Oligodendrocyte Myelin sheath Autophagy-lysosomal pathway Mechanistic target of rapamycin

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Digoxin Ameliorates Glymphatic Transport and Cognitive Impairment in a Mouse Model of chronic cerebral hypoperfusion

引用

Neuroscience Bulletin 2022年第2期38卷 181-199页

作者： Jie Cao Di Yao Rong Li Xuequn Guo Jiahuan Hao Minjie Xie Jia Li Dengji Pan Xiang Luo Zhiyuan Yu Minghuan Wang Wei Wang Department of Neurology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Pediatrics Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Respiratory Medicine Quanzhou First Hospital Affiliated to Fujian Medical UniversityQuanzhou 362000China Key Laboratory of Neurological Diseases of the Chinese Ministry of Education School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

The glymphatic system plays a pivotal role in maintaining cerebral homeostasis.chronic cerebral hypoperfusion,arising from small vessel disease or carotid stenosis,results in cerebrometabolic disturbances ultimately manifesting in white matter injury and cognitive dysfunction.However,whether the glymphatic system serves as a potential therapeutic target for white matter injury and cognitive decline during hypoperfusion remains unknown.Here,we established a mouse model of chronic cerebral hypoperfusion via bilateral common carotid artery stenosis.We found that the hypoperfusion model was associated with significant white matter injury and initial cognitive impairment in conjunction with impaired glym・phatic system function.The glymphatic dysfunction was associated with altered cerebral perfusion and loss of aquaporin 4 polarization.Treatment of digoxin rescued changes in glymphatic transport,white matter structure,and cognitive function.Suppression of glymphatic functions by treatment with the AQP4 inhibitor TGN-020 abolished this protective effect of digoxin from hypoperfusion injury.Our research yields new insight into the relationship between hemodynamics,glymphatic transport,white matter injury,and cognitive changes after chronic cerebral hypoperfusion.

关键词： chronic cerebral hypoperfusion Cognitive impairment Digoxin Glymphatic system White matter injury

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Hippocampal expression of synaptic structural proteins and phosphorylated cAMP response element-binding protein in a rat model of vascular dementia induced by chronic cerebral hypoperfusion

引用

Neural Regeneration Research 2012年第11期7卷 821-826页

作者： Hui Zhao Zhiyong Li Yali Wang Qiuxia Zhang School of Traditional Chinese Medicine Capital Medical University Beijing 100069 China China Minority Traditional Medical Center Minzu University of China Beijing 100081 China

The present study established a rat model of vascular dementia induced by chronic cerebral hypoperfusion through permanent ligation of bilateral common carotid arteries.At 60 days after modeling,escape latency and swimming path length during hidden-platform acquisition training in Morris water maze significantly increased in the model group.In addition,the number of accurate crossings over the original platform significantly decreased,hippocampal CA1 synaptophysin and growth-associated protein 43 expression significantly decreased,cAMP response element-binding protein expression remained unchanged,and phosphorylated cAMP response element-binding protein expression significantly decreased.Results suggested that abnormal expression of hippocampal synaptic structural protein and cAMP response element-binding protein phosphorylation played a role in cognitive impairment following chronic cerebral hypoperfusion.

关键词： cAMP response element-binding protein chronic cerebral hypoperfusion growth associated protein 43 learning and memory synaptophysin vascular dementia

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

3′-Daidzein sulfonate sodium protects against memory impairment and hippocampal damage caused by chronic cerebral hypoperfusion

引用

Neural Regeneration Research 2018年第9期13卷 1561-1567页

作者： Xiao Li Rui-Zhen Liu Qi Zeng Zhi-Hua Huang Jian-Dong Zhang Zong-Liang Liu Jing Zeng Hai Xiao Gannan Medical University Ganzhou Jiangxi Province China Department of Ultrasound First Affiliated Hospital of Gannan Medical University Ganzhou liangxi Province China Department of Pathology First Affiliated Hospital of Gannan Medical University Ganzhou Jiangxi Province China

3′-Daidzein sulfonate sodium（DSS） is a new synthetic water-soluble compound derived from daidzein,a soya isoflavone that plays regulatory roles in neurobiology.In this study,we hypothesized that the regulatory role of DSS in neurobiology exhibits therapeutic effects on hippocampal damage and memory impairment.To validate this hypothesis,we established rat models of chronic cerebral hypoperfusion（CCH） by the permanent occlusion of the common carotid arteries using the two-vessel occlusion method.Three weeks after modeling,rat models were intragastrically administered 0.1,0.2,and 0.4 mg/kg DSS,once a day,for 5 successive weeks.The Morris water maze test was performed to investigate CCH-induced learning and memory deficits.TUNEL assay was used to analyze apoptosis in the hippocampal CA1,CA3 regions and dentate gyrus.Hematoxylin-eosin staining was performed to observe the morphology of neurons in the hippocampal CA1,CA3 regions and dentate gyrus.Western blot analysis was performed to investigate the phosphorylation of PKA,ERK1/2 and CREB in the hippocampal PKA/ERK1/2/CREB signaling pathway.Results showed that DSS treatment greatly improved the learning and memory deficits of rats with CCH,reduced apoptosis of neurons in the hippocampal CA1,CA3 regions and dentate gyrus,and increased the phosphorylation of PKA,ERK1/2,and CREB in the hippocampus.These findings suggest that DSS protects against CCH-induced memory impairment and hippocampal damage possibly through activating the PKA/ERK1/2/CREB signaling pathway.

关键词： nerve regeneration learning and memory deficits chronic cerebral hypoperfusion 3＇-daidzein sulfonate sodium PKAIERK1/2/CREB signaling pathway neuroprotection hippocampus neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Panax ginseng extract attenuates neuronal injury and cognitive deficits in rats with vascular dementia induced by chronic cerebral hypoperfusion

引用

Neural Regeneration Research 2018年第4期13卷 664-672页

作者： Jun-De Zhu Jun-Jie Wang Xian-Hu Zhang Yan Yu Zhao-Sheng Kang Department of Anatomy School of Basic MedicineGuizhou Medical University

Panax ginseng is a slow-growing perennial plant.Panax ginseng extract has numerous biological activities,including antitumor,anti-inflammatory and antistress activities.Panax ginseng extract also has a cognition-enhancing effect in rats with alcohol-induced memory impairment.In this study,we partially occluded the bilateral carotid arteries in the rat to induce chronic cerebral hypoperfusion,a wellknown model of vascular dementia.The rats were then intragastrically administered 50 or 100 mg/kg Panax ginseng extract.Morris water maze and balance beam tests were used to evaluate memory deficits and motor function,respectively.Protein quantity was used to evaluate cholinergic neurons.Immunofluorescence staining was used to assess the number of glial fibrillary acidic protein-positive cells.Western blot assay was used to evaluate protein levels of vascular endothelial growth factor,basic fibroblast growth factor,Bcl-2 and Bax.Treatment with Panax ginseng extract for 8 weeks significantly improved behavioral function and increased neuronal density and VEGF and b FGF protein expression in the hippocampal CA3 area.Furthermore,Panax ginseng extract reduced the number of glial fibrillary acidic protein-immunoreactive cells,and it decreased apoptosis by upregulating Bcl-2 and downregulating Bax protein expression.The effect of Panax ginseng extract was dose-dependent and similar to that of nimodipine,a commonly used drug for the treatment of vascular dementia.These findings suggest that Panax ginseng extract is neuroprotective against vascular dementia induced by chronic cerebral hypoperfusion,and therefore might have therapeutic potential for preventing and treating the disease.

关键词： nerve regeneration Panax ginseng extract chronic cerebral hypoperfusion vascular dementia learning and memory vascular endothelial growth factor basic fibroblast growth factor apoptosis neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Effects of chronic cerebral hypoperfusion of beta- and gamma-secretase on learning and memory in rats

引用

Neural Regeneration Research 2010年第5期5卷 353-357页

作者： Xiaojuan Wang Hong Liu Liang Li Department of Pathology College of Basic Medical Sciences Capital Medical University Beijing 100069 China

BACKGROUND： chronic cerebral hypoxia and ischemia have been shown to be related to occurrence of sporadic Alzheimer＇s disease, and β- and y-secretase play an important role in the generation of β-amyloid protein. Early clinical symptoms in Alzheimer＇s disease patients include learning and memory deficits. OBJECTIVE： To measure learning and memory, as well as β- and β-secretase activities in the hippocampus of a cerebral ischemia/hypoxia rat model with chronic cerebral hypoperfusion. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Pathology, Capital Medical University from March to December, 2008. MATERIALS： β- and y-secretase activity kits were purchased from R ＆ D Systems, USA. METHODS： Male Sprague Dawiey rats, aged 23 weeks, were randomly assigned to model （n = 56） and sham-surgery （n = 46） groups. cerebral hypoperfusion rat models were established by bilateral common carotid occlusion. MAIN OUTCOME MEASURES： Morris water maze was used to test changes in escape latency and path length, and β- and y-secretase activities were measured on days 10, 30, 90, and 180 following surgery. RESULTS： Progressive cognitive impairment resulted from 30 days of chronic cerebral hypoperfusion, which lasted for 180 days after cerebral hypoperfusion. β-secretase activity was increased at 10 days after hypoperfusion, which continued until 180 days, with a 14.25% increase compared to the sham-surgery group; y-secretase activity was increased by 10.5%. CONCLUSION： chronic cerebral hypoperfusion results in impaired spatial memory and upregulated β- and y-secretase activities, which could play an important role in β-amyloid production.

关键词： chronic cerebral hypoperfusion β-amyloid β-secretase γ-secretase Alzheimer＇s disease brain injury neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Activation of glutamatergic neurons in the somatosensory cortex promotes remyelination in ischemic vascular dementia

引用

Fundamental Research 2024年第1期4卷 188-198页

作者： Yi-Ting Zhou Da-Dao An Yi-Xin Xu Ying Zhou Qing-Qing Li Hai-Bin Dai Xiang-Nan Zhang Yi Wang Min Lou Zhong Chen Wei-Wei Hu Department of Pharmacology and Department of Pharmacy of the Second Affiliated Hospital NHC and CAMS Key Laboratory of Medical NeurobiologySchool of Basic Medical SciencesCollege of Pharmaceutical SciencesZhejiang University School of MedicineHangzhou 310058China Department of Pharmacy Sir Run Run Shaw HospitalHangzhou 310012China Key Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province School of Pharmaceutical SciencesZhejiang Chinese Medical UniversityHangzhou 310053China Department of Neurology the Second Affiliated Hospital of Zhejiang UniversitySchool of MedicineHangzhou 310003China

chronic cerebral hypoperfusion can cause progressive demyelination as well as ischemic vascular dementia,however no effective treatments are available.Here,based on magnetic resonance imaging studies of patients with white matter damage,we found that this damage is associated with disorganized cortical structure.In a mouse model,optogenetic activation of glutamatergic neurons in the somatosensory cortex significantly promoted oligodendrocyte progenitor cell(OPC)proliferation,remyelination in the corpus callosum,and recovery of cognitive ability after cerebral hypoperfusion.The therapeutic effect of such stimulation was restricted to the upper layers of the cortex,but also spanned a wide time window after ischemia.Mechanistically,enhancement of glutamatergic neuron-OPC functional synaptic connections is required to achieve the protection effect of activating cortical glutamatergic neurons.Additionally,skin stroking,an easier method to translate into clinical practice,activated the somatosensory cortex,thereby promoting OPC proliferation,remyelination and cognitive recovery following cerebral hypoperfusion.In summary,we demonstrated that activating glutamatergic neurons in the somatosensory cortex promotes the proliferation of OPCs and remyelination to recover cognitive function after chronic cerebral hypoperfusion.It should be noted that this activation may provide new approaches for treating ischemic vascular dementia via the precise regulation of glutamatergic neuron-OPC circuits.

关键词： chronic cerebral hypoperfusion Optogenetic stimulation Oligodendrocyte progenitor cellIschemic vascular dementia Glutamatergic neuron Remyelination

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Therapeutic Benefit of Yangxue Qingnao Granule(养血清脑颗粒)on Cognitive Impairment Induced by chronic cerebral hypoperfusion in Rats

引用

Chinese Journal of Integrative Medicine 2011年第3期17卷 134-140页

作者：熊丽章军建孙冬刘晖 Department of Neurology Zhongnan Hospital of Wuhan University

Objective：To observe the therapeutic effect of Yangxue Qingnao Granule（养血清脑颗粒, YXQNG） on cognitive impairment induced by chronic cerebral hypoperfusion and to investigate its impact on oxidative stress,apoptosis,and the cholinergic system.Methods：Adult male Wistar rats were subjected to chronic cerebral hypoperfusion by permanent occlusion of bilateral common carotid arteries（2-VO）.Thirty rats were randomly assigned to one of the five treatment groups in a 1：1：1：1：1 ratio：sham operation plus normal saline treatment,2-VO plus normal saline treatment,2-VO plus YXQNG at a dose of 2 g·kg（-1）·d^（-1） or 4 g·kg（-1）·d^（-1）, or 2-VO plus rivastigmine 2 mgkg^（-1）·d^（-1）.The Morris water maze test was used to assess the spatial memory retrieval.Apoptosis,total antioxide capacity（T-AOC）,acetylcholine esterase（AchE） and choline acetyl transferase（ChAT） activities in the hippocampus and the cortex were investigated.Results：In the chronic cerebral hypoperfusion model,the 2-VO plus saline treatment resulted in impaired special learning as shown by the significantly prolonged escape latency and shorter swim time in the first quadrant as compared to the sham operation.The impairment was associated with apoptosis and significant decreases in T-AOC,AchE and ChAT activities in the hippocampus and the cortex.Treatment with YXQNG at either 2 g·kg（-1）·d^（-1） or 4 g·kg（-1）·d^（-1） dose,or rivastigmine resulted in significantly shorter escape latencies and longer swim time in the first quadrant.YXQNG at both doses,but not rivastigmine,had significant reduction in apoptosis,and significant increases in T-AOC and ChAT activity in both the hippocampus and the cortex.Unlike rivastigmine,neither dose of YXQNG showed significant reduction in AchE activity.Conclusions：YXQNG ameliorated cognitive impairment induced by chronic cerebral hypoperfusion.The protective effect may be mediated through its regulation of apoptosis and activities of T-AOC and ChAT in the hippocampus and cortex of the rats in the chronic cerebral hypoperfusion model,a mechani

关键词： Yangxue Qingnao Granule chronic cerebral hypoperfusion apoptosis total antioxide capacity acetylcholine esterase choline acetyl transferase

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

The effect of chronic cerebral hypoperfusion on β-amyloid peptide in rats' blood and brain

The effect of chronic cerebral hypoperfusion on β-amyloid p...

引用

中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： An-Feng XING,Le-Rong REN,Ye DING,Jue WANG,Liang LI Department of Pathology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China

Objective To investigate the effect of chronic cerebral hypoperfusion on β-amyloid peptide(Aβ) which plays a very important role in the onset of Alzheimer’s disease,chronic cerebral hypoperfusion rat model was employed to observe the changes of Aβin rats’s blood and brain,the distributions of Aβsubtype in the brain,the rats’ learning and memory capability and the amyloidosis of the blood vessels.Methods Male Sprague-Dawley rats,approximately 10 months of age,were randomly divided into model groups(M groups) and control groups(C groups).Permanent bilateral carotid occlusion(2-VO) was done to lead to sustained chronic cerebral ischemia to the model rats.Age-matched control groups were performed surgery without bilateral carotid occlusion.The rats were devided into 10 d group,30 d group,90 d group and 180 d group.Then the following experiments were fulfilled:(1) Spatial learning and memory capability were tested by Morris water maze;(2) Weight and volume of the rats’ brain was measured;(3) Radioimmunoassay was employed to test the levels of Aa in serum,cortex and hippocampus;(4) The expression of APP in the extract from homogenate of hippocampus and cortex of rats were evaluated by western-blot;(5) Histomorphology:Hematoxylin-eosin staining(HE) was processed to observe the general morphological changes of the rats’s brain;Immunohistochemistry was processed to observe the distribution and expression of APP,Aβ and Aβ;And the amyloidosis of the blood vessels was observed by Congo red dyeing.Results(1) Escaping latency time and swimming distance was postponed initially in model group after 30 days of hypoperfusion compared with control group(Phypoperfusion(P<0.05 and P<0.01,respectively). (2) The weight of the rats’ brain in 10 d model group was more than that of control group(P<0.05).(3) The content of Aβin the serum was more signigicantly increased in 10 d、30 d、90 d and 180 d in model groups compared to that of

关键词： chronic cerebral hypoperfusion Alzheimer’s disease β-amyloid peptide β-amyloid precursor protein

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Angelica compensates cognitive impairment by regulating brain-derived neurotrophic factor expression in hippocampus of the chronic cerebral hypoperfusion rat

Angelica compensates cognitive impairment by regulating brai...

引用

第十届全国心理学学术大会

作者： Ping Zheng Department of Psychology, Central China Normal University, Wuhan 430079, China.

chronic cerebral hypoperfusion causes cognitive impairment, the aim of the present research was to study molecule basis underlying this pathophysiological state and neuroprotective agent acting on it. The rats were divided into three groups: angelica treatment group, saline administration group and sham operation group. Permanent occlusion of bilateral common carotid occlusion (2-VO) was used to induce a chronic reduction of cerebral blood flow to the brain of rat. Angelica treatment group were given a single dose of angelica decoction (8ml/kg per day) by gastric garage for two months after 2-VO surgery completed.

关键词： chronic cerebral hypoperfusion angelica NGF BDNF cognitive impairment

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：