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Hypothermia selectively protects the anterior forebrain mesocircuit during global cerebral ischemia

Neural Regeneration Research 2022年第7期17卷 1512-1517页

作者： Xiao-Hua Wang Wei Jiang Si-Yuan Zhang Bin-Bin Nie Yi Zheng Feng Yan Jian-Feng Lei Tian-Long Wang Department of Anesthesiology Xuanwu HospitalCapital Medical UniversityBeijingChina National Clinical Research Center for Geriatric Disorders BeijingChina Department of Anesthesiology Third Medical Center of People’s Liberation Army General HospitalBeijingChina Daxing Hospital Affiliated to Capital Medical University BeijingChina Beijing Engineering Research Center of Radiographic Techniques and Equipment Institute of High Energy PhysicsChinese Academy of SciencesBeijingChina School of Nuclear Science and Technology University of Chinese Academy of SciencesBeijingChina Neuroprotection Research Laboratory Departments of Radiology and NeurologyMassachusetts General Hospital and Harvard Medical SchoolCharlestownMAUSA Cerebrovascular Research Center Xuanwu HospitalCapital Medical UniversityBeijingChina

Hypothermia is an important protective strategy against global cerebral ischemia following cardiac arrest.However,the mechanisms of hypothermia underlying the changes in different regions and connections of the brain have not been fully elucidated.This study aims to identify the metabolic nodes and connection integrity of specific brain regions in rats with global cerebral ischemia that are most affected by hypothermia treatment.18F-fluorodeoxyglucose positron emission tomography was used to quantitatively determine glucose metabolism in different brain regions in a rat model of global cerebral ischemia established at 31–33℃.Diffusion tensor imaging was also used to reconstruct and explore the brain connections involved.The results showed that,compared with the model rats established at 37–37.5℃,the rat models of global cerebral ischemia established at 31–33℃had smaller hypometabolic regions in the thalamus and primary sensory areas and sustained no obvious thalamic injury.Hypothermia selectively preserved the integrity of the anterior forebrain mesocircuit,exhibiting protective effects on the brain during the global cerebral ischemia.The study was approved by the Institutional Animal Care and Use Committee at Capital Medical University(approval No.XW-AD318-97-019)on December 15,2019.

关键词： anterior forebrain mesocircuit cardiac arrest corpus callosum global cerebral ischemia hypometabolic areas hypothermia magnetic resonance imaging positron emission tomography prefrontal cortex rats thalamus

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Dynamic expression of cerebral cortex and hippocampal glutamate transporters in a rat model of chest compression-induced global cerebral ischemia

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Neural Regeneration Research 2012年第2期7卷 125-130页

作者： Qinhua Guo Jin Lan Weiqiao Zhang Pin Guo Liemei Guo Zhiqiang Li Yongming Qiu Department of Neurosurgery Renji Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200127 China Central Hospital of Fengxian District Shanghai Neurological Research Institute of Anhui University of Science ＆ Technology Shanghai201400 China

The present study established a rat model of global cerebral ischemia induced by chest compression for six minutes to dynamically observe expressional changes of three glutamate transporters in the cerebral cortex and hippocampus. After 24 hours of ischemia, expression of glutamate transporter-1 significantly decreased in the cerebral cortex and hippocampus, which was accompanied by neuronal necrosis. At 7 days post-ischemia, expression of excitatory amino acid carrier 1 decreased in the hippocampal CA1 region and cortex, and was accompanied by apoptosis Expression of glutamate-aspartate transporter remained unchanged at 6 hours 7 days after ischemia. These results suggested that glutamate transporter levels were altered at different periods of cerebral ischemia.

关键词： apoptosis excitatory amino acid carrier 1 global cerebral ischemia glutamate-aspartate transporter glutamate transporter glutamate transporter-1 neuroprotection

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Ischemic preconditioning partially suppresses and postpones integrin α_Vβ_3 mRNA expression following transient global cerebral ischemia in C57BL/6 mice

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Neural Regeneration Research 2010年第23期5卷 1782-1786页

作者： Mei Liu Xiaomeng Ma Xiaohong Chen Ying Jiang Aimin Wu Fuhua Peng Yingying Liu Rongbiao Pi Department of Neurology the Third Affiliated Hospital of Sun Yat-sen University Guangzhou 510630 Guangdong Province China Department of Pharmacology and Toxicology School of Pharmaceutical Sciences Sun Yat-sen University Guangzhou 510020 Guangdong Province China

Previous studies of integrin αvβ3 have focused on ischemic brain damage, although the role of integrin αvβ3 in ischemic preconditioning （IP） has rarely been reported. The present study analyzed the effects of IP on integrin αvβ3 mRNA expression following cerebral ischemia through the use of hematoxylin-eosin staining and real-time quantitative polymerase chain reaction techniques. Integrin avid3 mRNA expression in the ischemia group peaked at 24 hours after ischemia-reperfusion. In the IP ＋ ischemia group, integrin αvβ3 mRNA expression increased after 24 hours, but remained significantly less than the ischemia group, and expression continued to increase until 7 days after ischemiaJreperfusion. These results demonstrate that IP effectively attenuated upregulation of integrin αvβ3 mRNA expression at 24 hours after ischemia.

关键词： integrin αvβ3 ischemic preconditioning ischemic tolerance global cerebral ischemia blood-brain barrier： mice

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Protective effects of iptakalim,a novel ATP-sensitive potassium channel opener,on global cerebral ischemia-evoked insult in gerbils

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Acta Pharmacologica Sinica 2006年第6期27卷 665-672页

作者： Hua CHEN~(2,4)Yong YANG~(2,4)Hong-hong YAO~2 Xing-chun TANG~2 Jian-hua DING~2 Hai WANG~3 Gang HU~(2,5)2 Laboratory of Neuropharmacology,Department of Anatomy,Histology and Pharmacology,Nanjing Medical University,Nanjing 210029,China 3 Department of Cardiovascular Pharmacology,Beijing Institute of Pharmacology and Toxicology,Beijing 100850,China LaboratoryofNeuropharmacology DepartmentofAnatomyHistologyandPharmacologyNanjingMedicalUniversityNanjing210029China DepartmentofCardiovascularPharmacology BeijingInstituteofPharmacologyandToxicologyBeijing100850Ch

Aim:To investigate the protective role of iptakalim,a novel ATP sensitive potas-sium channel opener,on global cerebral ischemia-evoked insult in gerbils andglutamate-induced PC 12 cell injury.Methods:global cerebral ischemia was in-duced by occluding the bilateral common carotid arteries in gerbils for 5 min.Theopen field maze and T-maze were employed to investigate the experimental thera-peutic value of iptakalim on ischemic brain insult(n=8).The pyramidal cells in thehippocampal CA1 regions were counted to assess the protective effects ofiptakalim.Glutamate released from the gerbil hippocampus and PC12 cells weredetermined by HPLC.Intracellular calcium was measured by Fluo-3 AM with ABio-Rad Radiance 2100TM confocal system in conjunction with a Nikon TE300microscope.Astrocyte glutamate uptake measurements were determined by liq-uid scintillation counting.Results:Iptakalim(0.5-4.0 mg/kg per day,ip)couldreduce the high locomotor activity evoked by ischemia and improve global cere-bral ischemia-induced working memory impairments.Histological studies revealedthat iptakalim could increase the survival neuron in the hippocampus CA1 zone ina dose-dependent manner.Moreover,iptakalim could reverse ischemia-evokedincreases of glutamate in the hippocampus of gerbils.In an in vitro study,iptakalimprotected PC12 cells against glutamate-induced excitotoxicity,reduced the[Ca2+]iincreases,and enhanced the glutamate uptake activity of primary culturedastrocytes.Conclusions:Iptakalim plays a key role in preventing global cerebralischemia-evoked insults in gerbils and glutamate-induced PC12 cell injury by anti-excitotoxicity.Iptakalim might be a promising novel candidate for the preventionand/or treatment of stroke.

关键词： ATP-sensitive potassium channel opener iptakalim global cerebral ischemia neuroprotection excitotoxicity

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Agmatine reduces nitric oxide synthase expression and peroxynitrite formation in the cerebral cortex in a rat model of transient global cerebral ischemia

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Neural Regeneration Research 2010年第23期5卷 1773-1781页

作者： Chin Hee Mun Won Taek Lee Kyung Ah Park Jong Eun Lee Department of Anatomy Yonsei University College of Medicine Brain Korea 21 Project for Medical Science Yonsei University College of Medicine

Agmatine, an analog of L-arginine, is an endogenous substance synthesized by arginine decarboxylase, which has been shown to possess neuroprotective effects following brain ischemia. Nitric oxide is generated by sequential oxidation of the guanidinium group in L-arginine, and agmatine might protect the brain from ischemic injury by interfering with nitric oxide signaling. This study investigated the effects of agmatine on cerebral cortex neuronal injury following transient global cerebral ischemia and also detected nitric oxide synthase expression and peroxynitrite formation. Results demonstrated that intraperitoneal injection of agmatine in global cerebral ischemia/reperfusion alleviated ischemia/reperfusion-induced cerebral cortical cortex neuronal injury and cellular apoptosis, decreased neuronal and inducible nitric oxide synthase expression at 24, 48, and 72 hours following global cerebral ischemia and reperfusion, and greatly inhibited nitrotyrosine levels, which reflect the amount of peroxynitrite formed. These findings indicated that agmatine alleviates cerebral cortex neuronal injury following global cerebral ischemia and decreases nitric oxide synthase expression and peroxynitrite formation following ischemia/repeffusion.

关键词： agmatine global cerebral ischemia cerebral cortex nitric oxide nitric oxide synthase neuroprotection

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Role of 5-lipoxygenase in hippocampal neuron damage following global cerebral ischemia in rats

Role of 5-lipoxygenase in hippocampal neuron damage followin...

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中国药理学会第十一次全国学术会议

作者： CHEN Wen-jian,LI Cheng-tan,ZHAO Jian-bo,ZHANG Xiao-yan,LIN Xiao-xia,ZHANG Li-hui (Hangzhou Key Laboratory of Neurobiology and Department of Pharmacology,School of Basic Medicine,Hangzhou Normal University,Hangzhou 310036,China)

OBJECTIVE To determine spatio-temporal properties of 5-lipoxygenase(5-LOX) expression and the effect of zileuton, a selective 5-LOX inhibitor,on the hippocampal neuron injury following global cerebral ischemia(GCI).METHODS GCI was induced by bilateral common carotid artery occlusion combined with hypotension in rats.5-LOX expression was detected by Western blot analyses and 5-LOX localization was visualized by immunohistochemistry and double immunoflurescence.The 5-LOX inhibitor zileuton(10,30,50 mg·kg) were orally administered.RESULTS The 5-LOX expression was significantly upregulated in the hippocampus 1,3 and 7 d(peaked at 3 d) after ischemia.In the hippocampal CA1 region,5-LOX protein was primarily localized in the neurons.The 5-LOX inhibitor zileuton(30,50 mg·kg) markedly reduced hippocampal CA1 neuron damage at 3 d after ischemia. Protective effect of zileuton(30 mg·kg,7 consecutive days) is still evident 14 d after the ischemia episode.CONCLUSION 5-LOX is involved in global cerebral ischemic damage,the 5-LOX selective inhibitor zileuton possesses neuroprotective effect on neuronal damage in the rat hippocampus following GCI.

关键词： global cerebral ischemia hippocampus neuron 5-lipoxygenase zileuton

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Isoflurane preconditioning induces neuroprotection by attenuating ubiquitin-conjugated protein aggregation after transient global cerebral ischemia in mouse

Isoflurane preconditioning induces neuroprotection by attenu...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Hao-Peng ZHANG,Hai-Long DONG*,Su-Bin XIAO~1,Rui MA,Li-Ze Xiong~* Department of Anesthesiology,Xijing Hospital,Fourth Military Medical University,Xi’an 710032,China

Objective The aim of this study is to clarify the role of ubiquitin-conjugated protein aggregation in the formation of neuroprotective effect of isoflurane preconditioning on the transient global cerebral ischemia-reperfusion injury in the C57BL/6 mouse.Methods All animals were randomly assigned to two groups(isoflurane preconditioning group and control group,n=36 in each).Mice in isoflurane preconditioning(IP) group were placed in a chamber and pretreated with isoflurane(1.2%isoflurane,98%O

关键词： Ubiquitin-Proteasome isoflurane preconditioning C57BL/6 mouse global cerebral ischemia

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Effect of bFGF on endogenous NSCs in rat hippocampus with global cerebral ischemia-reperfusion

Effect of bFGF on endogenous NSCs in rat hippocampus with gl...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Ming-Xin REN,Yi-Wei GUO,Zhi-Bo FENG~* Department of Anatomy,Xinxiang Medical University,Xinxiang 453003,China

Objective Study the effect of bFGF on endogenous neural stem cell proliferation,migration and differentiation in rats hippocampus with global brain ischemia-reperfusion.Methods Male Sprague-Dawley rats (250-300 g ) were divided into there groups:sham operation group(A),operation group(B),bFGF group(C).The global brain ischemia-reperfusion models were established,and then the bFGF was injected into the lateral ventricle in group C.The doses of 5μl(0.1μg/μl) was administrated before the model operation,and once every two days after operation.The rat brains were acquired at 3 d,7 d,11 d,15 d with intraperitoneal injection of BrdU 1 d before animal sacrifice.HE and immunohistochemistry were used to observe the pathological changes and the expression of BrdU and Nestin in cerebral hippocampus and cortex.RT-PCR was used to measure the NSE mRNA in brain tissue.Results(1) HE staining:There were a lot of degenerated and necrotic neurons and the bodies were shrunken with karyopycnosis and chrornatospherite vanished.In group C the number of survival neurons was increased.(2) Immunohistochemistry:In group A,there were few positive cells in hippocampus and cerebral cortex.Compared with group A,the expression of BrdU and Nestin was increased significantly at 3 day in B,C group,peaked at 7 day in B group and at 11 day in C group,then began to decrease.Compared with model group,the number of BrdU-positive and Nestin-positive cells were increased significantly at each time point in group C(Pglobal cerebral ischemia and reperfusion.(2) The proliferation of endogenous neural stem cells in situ can be promoted and extended by global cerebral ischemia and reperfusion of rat.And bFGF on promoting endogenous neural stem cells differentiated into neurons.

关键词： global cerebral ischemia endogenous neural stem cells bFGF rat

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Lithium improves the behavioral disorder in rats subjected to transient global cerebral ischemia

Lithium improves the behavioral disorder in rats subjected t...

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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： Xue-Bo YAN,Shan-Shan WANG,Hai-Long HOU,Rui JI,Jiang-Ning ZHOU Hefei National Laboratory for Physical Sciences at Microscale and Department of Neurobiology and Biophysics, School of Life Science,University of Science and Technology of China,Hefei,230027,China

＜正＞Previous study has indicated that chronic treatment with lithium protects brain against ischemic injury by reducing apoptotic death.To investigate whether lithium improves the behavioral disorder induced by transient global cerebral ischemia,we examined the effects of lithium treatment on the performance of rats in a set of behavioral tests,i.e. beam balance,elevated plus maze（EPM）,open field and Morris water maze.Our results showed that lithium attenuated the worse general ’well-being’ and the worse performance in beam balance,and hyperactivity in EPM and open field,including increased open arm entries,time spent in the open arms,squares crossed,rearing and grooming over 7 days after 15 minutes ischemia,which were induced by four-vessel occlusion in Sprague-Dawley rats.Moreover,Lithium improved the injured spatial learning and memory ability in Morris water maze at post-ischemic day 8 and 9.Histological analysis displayed that it decreased obviously cell death in hippocampal CA1 region.Our study further confirmed the protective role of lithium in the ischemia-reperfusion injury and suggested that lithium might be a helpful therapeutic approach to the treatment of stroke combining with other neuroprotective agents.

关键词： lithium global cerebral ischemia hyperactivity learning and memory hippocampus rats

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Ischemic preconditioning protects against ischemic brain injury

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Neural Regeneration Research 2016年第5期11卷 765-770页

作者： Xiao-meng Ma Mei Liu Ying-ying Liu Li-li Ma Ying Jiang Xiao-hong Chen Department of Neurology the Third Affiliated Hospital of Sun Yat-sen University

In this study, we hypothesized that an increase in integrin αβand its co-activator vascular endothelial growth factor play important neuroprotective roles in ischemic injury. We performed ischemic preconditioning with bilateral common carotid artery occlusion for 5 minutes in C57BL/6J mice. This was followed by ischemic injury with bilateral common carotid artery occlusion for 30 minutes. The time interval between ischemic preconditioning and lethal ischemia was 48 hours. Histopathological analysis showed that ischemic preconditioning substantially diminished damage to neurons in the hippocampus 7 days after ischemia. Evans Blue dye assay showed that ischemic preconditioning reduced damage to the blood-brain barrier 24 hours after ischemia. This demonstrates the neuroprotective effect of ischemic preconditioning. Western blot assay revealed a significant reduction in protein levels of integrin αβ, vascular endothelial growth factor and its receptor in mice given ischemic preconditioning compared with mice not given ischemic preconditioning 24 hours after ischemia. These findings suggest that the neuroprotective effect of ischemic preconditioning is associated with lower integrin αβand vascular endothelial growth factor levels in the brain following ischemia.

关键词： nerve regeneration brain injury integrin αvβ3 vascular endothelial growth factor vascular endothelial growth factor receptor vascular endothelial growth factor receptor-2 fetal liver kinase 1 ischemic preconditioning ischemic tolerance global cerebral ischemia cerebral ischemia cerebral infarction NSFC grant neural regeneration

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