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cerebral ischemia mechanism

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https://www.readbyqxmd.com/read/29160389/protective-effect-of-ischemic-preconditioning-on-myocardium-against-remote-tissue-injury-following-transient-focal-cerebral-ischemia-in-diabetic-rats
#1
Meltem Kumas, Ozge Altintas, Ersin Karatas, Abdurrahim Kocyigit
BACKGROUND: Remote ischemic preconditioning (IPreC) could provide tissue-protective effect at a remote site by anti-inflammatory, neuronal, and humoral signaling pathways. OBJECTIVES: The aim of the study was to investigate the possible protective effects of remote IPreC on myocardium after transient middle cerebral artery occlusion (MCAo) in streptozotocin- induced diabetic (STZ) and non-diabetic rats. METHODS: 48 male Spraque Dawley rats were divided into eight groups: Sham, STZ, IPreC, MCAo, IPreC+MCAo, STZ+IPreC, STZ+MCAo and STZ+IPreC+MCAo groups...
November 13, 2017: Arquivos Brasileiros de Cardiologia
https://www.readbyqxmd.com/read/29159732/the-pgc-1%C3%AE-activator-zln005-ameliorates-ischemia-induced-neuronal-injury-in-vitro-and-in-vivo
#2
Yazhou Xu, John Alimamy Kabba, Wenchen Ruan, Yunjie Wang, Shunyi Zhao, Xiaoyue Song, Luyong Zhang, Jia Li, Tao Pang
Oxidative stress is a great challenge to neurons following cerebral ischemia. PGC-1α has been shown to act as a potent modulator of oxidative metabolism. In this study, the effects of ZLN005, a small molecule that activate PGC-1α, against oxygen-glucose deprivation (OGD)- or ischemia-induced neuronal injury in vitro and in vivo were investigated. Transient middle cerebral artery occlusion (tMCAO) was performed in rats and ZLN005 was administered intravenously at 2 h, 4 h, or 6 h after ischemia onset. Infarct volume and neurological deficit score were detected to evaluate the neuroprotective effects of ZLN005...
November 20, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/29142624/significances-and-outcomes-of-mechanical-thrombectomy-for-acute-infarction-in-very-elderly-patients-a-single-center-experience
#3
Dong Hun Kim, Sang Uk Kim, Jae Hoon Sung, Dong Hoon Lee, Ho Jun Yi, Sang Won Lee
Objective: Mechanical thrombectomy is increasingly being used for the treatment of acute ischemic stroke. The population over 80 years of age is growing, and many of these patients have acute infarction; however, these patients are often excluded from clinical trials, so the aim of this study was to compare the functional outcomes and complication rates in very elderly patients (age ≥80 years) and aged patients (60-79 years) treated with mechanical thrombectomy. Methods: Between January 2010 and June 2015, we retrospectively reviewed 113 senior patients (over 60 years old) treated at our institution for acute ischemic stroke with mechanical thrombectomy...
November 2017: Journal of Korean Neurosurgical Society
https://www.readbyqxmd.com/read/29138801/vitamin-d-receptor-activation-influences-the-erk-pathway-and-protects-against-neurological-deficits-and-neuronal-death
#4
Jie Yuan, Xin Guo, Zhengang Liu, Xiuqin Zhao, Yan Feng, Sixin Song, Changmeng Cui, Pei Jiang
Previous studies have demonstrated that global cerebral ischemia (GCI) causes neurological deficits and neuronal cell apoptosis. Calcitriol, a biologically active metabolite of vitamin D, exerts its endocrinological influence via nuclear vitamin D receptor. It is being assessed as an emerging therapeutic strategy in models of various medical conditions, including acute brain injury. The purpose of the present study was to investigate the neuroprotective effects of calcitriol on GCI and further refine the potential underlying mechanisms...
November 9, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29137683/tanshinone-i-alleviates-motor-and-cognitive-impairments-via-suppressing-oxidative-stress-in-the-neonatal-rats-after-hypoxic-ischemic-brain-damage
#5
Chunfang Dai, Yannan Liu, Zhifang Dong
Neonatal hypoxia-ischemia is one of the main reasons that cause neuronal damage and neonatal death. Several studies have shown that tanshinone I (TsI), one of the major ingredients of Danshen, exerts potential neuroprotective effect in adult mice exposed to permanent left cerebral ischemia. However, it is unclear whether administration of TsI has neuroprotective effect on neonatal hypoxic-ischemic brain damage (HIBD), and if so, the potential mechanisms also remain unclear. Here, we reported that treatment with TsI (5 mg/kg, i...
November 14, 2017: Molecular Brain
https://www.readbyqxmd.com/read/29135346/cerebral-artery-myogenic-reactivity-the-next-frontier-in-developing-effective-interventions-for-subarachnoid-hemorrhage
#6
Darcy Lidington, Jeffrey T Kroetsch, Steffen-Sebastian Bolz
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebral event that kills or debilitates the majority of those afflicted. The blood that spills into the subarachnoid space stimulates profound cerebral artery vasoconstriction and consequently, cerebral ischemia. Thus, once the initial bleeding in SAH is appropriately managed, the clinical focus shifts to maintaining/improving cerebral perfusion. However, current therapeutic interventions largely fail to improve clinical outcome, because they do not effectively restore normal cerebral artery function...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29133510/single-cell-immuno-laser-microdissection-coupled-to-label-free-proteomics-to-reveal-the-proteotypes-of-human-brain-cells-after-ischemia
#7
Teresa García-Berrocoso, Víctor Llombart, Laura Colàs-Campàs, Alexandre Hainard, Virginie Licker, Anna Penalba, Laura Ramiro, Alba Simats, Alejandro Bustamante, Elena Martínez-Saez, Francesc Canals, Jean-Charles Sanchez, Joan Montaner
Cerebral ischemia entails rapid tissue damage in the affected brain area causing devastating neurological dysfunction. How each component of the neurovascular unit contributes or responds to the ischemic insult in the context of the human brain has not been solved yet. Thus, the analysis of the proteome is a straightforward approach to unraveling these cell proteotypes.In this study, post-mortem brain slices from ischemic stroke patients were obtained corresponding to infarcted (IC) and contralateral (CL) areas...
November 13, 2017: Molecular & Cellular Proteomics: MCP
https://www.readbyqxmd.com/read/29129468/inhibition-of-rac1-ameliorates-neuronal-oxidative-stress-damage-via-reducing-bcl-2-rac1-complex-formation-in-mitochondria-through-pi3k-akt-mtor-pathway
#8
Yundan Pan, Na Wang, Pingping Xia, E Wang, Qulian Guo, Zhi Ye
Although the neuroprotective effects of Rac1 inhibition have been reported in various cerebral ischemic models, the molecular mechanisms of action have not yet been fully elucidated. In this study, we investigated whether the inhibition of Rac1 provided neuroprotection in a diabetic rat model of focal cerebral ischemia and hyperglycemia-exposed PC-12 cells. Intracerebroventricular administration of lentivirus expressing the Rac1 small hairpin RNA (shRNA) and specific Rac1 inhibitor NSC23766 not only decreased the infarct volumes and improved neurologic deficits with a correlated significant activation of mitochondrial DNA specific proteins, such as OGG1 and POLG, but also elevated Bcl-2 S70 phosphorylation in mitochondria...
November 10, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/29128627/inhibition-of-jak1-by-microrna-708-promotes-sh-sy5y-neuronal-cell-survival-after-oxygen-and-glucose-deprivation-and-reoxygenation
#9
Chao Huang, Haitao Zhou, Xiangyang Ren, Junfang Teng
MicroRNAs mediates gene expression in various diseases. Studies have shown that aberrant expression of miRNAs affected cerebral protection. In this study, we have investigated the effects of microRNA-708 (miR-708) on cell survival of oxygen and glucose-deprived reoxygenation (OGD/R) human neuroblastoma cells (SH-SY5Y) and explored whether miR-708 inhibited neuronal death by targeting JAK1. In vitro model of ischemia was used to investigate the neuroprotective functions of miR-708. MiR-708 mimics/siJAK1 transfected SH-SY5Y cells were treated with OGD...
November 9, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/29128308/oxidative-stress-and-dna-damage-after-cerebral-ischemia-potential-therapeutic-targets-to-preserve-the-genome-and-improve-stroke-recovery
#10
REVIEW
Peiying Li, R Anne Stetler, Rehana K Leak, Yejie Shi, Yan Li, Weifeng Yu, Michael V L Bennett, Jun Chen
The past two decades have witnessed remarkable advances in oxidative stress research, particularly in the context of ischemic brain injury. Oxidative stress in ischemic tissues compromises the integrity of the genome, resulting in DNA lesions, cell death in neurons, glial cells, and vascular cells, and impairments in neurological recovery after stroke. As DNA is particularly vulnerable to oxidative attack, cells have evolved the ability to induce multiple DNA repair mechanisms, including base excision repair (BER), nucleotide excision repair (NER) and non-homogenous endpoint jointing (NHEJ)...
November 8, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29125039/astrocyte-autophagy-flux-protects-neurons-against-oxygen-glucose-deprivation-and-ischemic-reperfusion-injury
#11
Xue Liu, Fengfeng Tian, Shiquan Wang, Feng Wang, Lize Xiong
The role of autophagy varies with the type of acute brain injury. In general, autophagy mediates a clear neuroprotective effect in intoxication caused by various psychoactive agents, subarachnoid hemorrhage and spinal cord injury. In contrast, autophagic cell death has also been reported to actively contribute to neuronal loss in neonatal hypoxic ischemic encephalopathy. However, it still remains to be determined whether autophagy pays a cytoprotective or a cytotoxic role in stroke. Previous studies focused primarily on the role of neurons rather than the role of astrocytes in brain injury...
November 10, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/29123466/neuroprotective-effect-of-%C3%AE-caryophyllene-on-cerebral-ischemia-reperfusion-injury-via-regulation-of-necroptotic-neuronal-death-and-inflammation-in-vivo-and-in-vitro
#12
Mei Yang, Yongjiu Lv, Xiaocui Tian, Jie Lou, Ruidi An, Qian Zhang, Minghang Li, Lu Xu, Zhi Dong
Necrotic cell death is a hallmark feature of ischemic stroke and it may facilitate inflammation by releasing intracellular components after cell-membrane rupture. Previous studies reported that β-caryophyllene (BCP) mitigates cerebral ischemia-reperfusion (I/R) injury, but the underlying mechanism remains unclear. We explored whether BCP exerts a neuroprotective effect in cerebral I/R injury through inhibiting necroptotic cell death and inflammation. Primary neurons with and without BCP (0.2, 1, 5, 25 μM) treatment were exposed to oxygen-glucose deprivation and re-oxygenation (OGD/R)...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29122651/downregulation-of-lipocalin-2-and-bim-expression-after-remote-limb-preconditioning-in-the-ischemic-rat-brain
#13
Mingli Liu, Jing Chen, Shufan Zhang, Chuancheng Ren
Although it has been proved that remote limb preconditioning (RPC) can exert neurological protection effects after ischemic cerebral stroke (ICS), the underlying mechanisms of RPC still need to be elucidated for its better transformation to clinical application. Lipocalin-2 (LCN2) was upregulated after cerebral ischemia and mediated reperfusion injury in the models of ischemic stroke. So here, we investigated that whether RPC could downregulate the levels of LCN2 protein and its receptor resulting from cerebral ischemia reperfusion (I/R) injury...
November 6, 2017: Brain Research
https://www.readbyqxmd.com/read/29119925/post-treatment-with-a-hydrogen-sulfide-donor-limits-neuronal-injury-and-modulates-potassium-voltage-gated-channel-subfamily-d-member-2-kv4-2-and-potassium-channel-interacting-protein-3-kchip3-during-transient-global-cerebral-ischemia
#14
Cheng-Ping Bai, ChenLiang Zhao, Lijuan Shen
BACKGROUND: Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains largely unknown. OBJECTIVE: We aimed to investigate the neuroprotective effect of NaHS post-conditioning against transient global cerebral ischemia (tGCI)-induced hippocampal CA1 injury and its underlying molecular mechanism. METHODS: A tGCI rat model was established using the four-vessel occlusion method for 15 min of ischemia...
November 7, 2017: Current Neurovascular Research
https://www.readbyqxmd.com/read/29117499/preclinical-chorioamnionitis-dysregulates-cxcl1-cxcr2-signaling-throughout-the-placental-fetal-brain-axis
#15
REVIEW
Tracylyn R Yellowhair, Shahani Noor, Jessie R Maxwell, Christopher V Anstine, Akosua Y Oppong, Shenandoah Robinson, Erin D Milligan, Lauren L Jantzie
In the United States, perinatal brain injury (PBI) is a major cause of infant mortality and childhood disability. For a large proportion of infants with PBI, central nervous system (CNS) injury begins in utero with inflammation (chorioamnionitis/CHORIO) and/or hypoxia-ischemia. While studies show CHORIO contributes to preterm CNS injury and is also a common independent risk factor for brain injury in term infants, the molecular mechanisms mediating inflammation in the placental-fetal-brain axis that result in PBI remain a gap in knowledge...
November 5, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/29115923/neuroprotective-effect-of-neuroserpin-in-non-tpa-induced-intracerebral-hemorrhage-mouse-models
#16
Wei Li, Tetsuya Asakawa, Sha Han, Baoguo Xiao, Hiroki Namba, Chuanzhen Lu, Qiang Dong, Liang Wang
BACKGROUND: The neuroprotective effects of neuroserpin (NSP) have been well documented in both patients and animal models with cerebral ischemia; however, have never been investigated in hemorrhagic stroke. The aim of this study is to verify the neuroprotection of NSP in the non-tPA-induced intracerebral hemorrhage (ICH) mouse model. METHODS: C57BL/6J male mice (n = 198) were involved in this study. ICH models were established with infusion of autologous blood into the brain parenchyma...
November 7, 2017: BMC Neurology
https://www.readbyqxmd.com/read/29115485/effect-of-willed-movement-training-on-neurorehabilitation-after-focal-cerebral-ischemia-and-on-the-neural-plasticity-associated-signaling-pathway
#17
Zhi-Wen Zhou, Qi-Dong Yang, Qing-Ping Tang, Jie Yang, Rong-Jing Guo, Wen Jiang
Neurorehabilitation training is a therapeutic intervention for the loss of neural function induced by focal cerebral ischemia, however, the effect varies depending on the neurorehabilitation exercises. Willed movement (WM) training is defined as task‑oriented training, which increases enthusiasm of patients to accomplish a specific task. The current study was performed to the evaluate effect of WM training on neurorehabilitation following focal cerebral ischemia, and further investigate the influence on neural plasticity‑associated signaling pathway...
November 3, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29115424/cornin-protects-sh%C3%A2-sy5y-cells-against-oxygen-and-glucose-deprivation%C3%A2-induced-autophagy-through-the-pi3k-akt-mtor-pathway
#18
Changling Ding, Jie Zhang, Baoyuan Li, Zhaoxing Ding, Wenna Cheng, Fei Gao, Ye Zhang, Yangyang Xu, Shuping Zhang
It has been reported that cornin may reduce neuronal death during cerebral ischemia; however, little is known about the molecular mechanism of the role of corninin autophagy in SH‑SY5Y neuronal cells. In the present study, oxygen‑glucose deprivation (OGD)‑treated cells were used as a cerebral ischemia model in vitro. The results demonstrated that cornin was able to reduce neuronal cell loss, increase the apoptosis regulator Bcl‑2/apoptosis regulator BAX ratio, and decrease the protein levels of caspase‑3...
October 25, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29114092/inhibition-of-cd147-cluster-of-differentiation-147-ameliorates-acute-ischemic-stroke-in-mice-by-reducing-thromboinflammation
#19
Rong Jin, Adam Y Xiao, Rui Chen, D Neil Granger, Guohong Li
BACKGROUND AND PURPOSE: Inflammation and thrombosis currently are recognized as critical contributors to the pathogenesis of ischemic stroke. CD147 (cluster of differentiation 147), also known as extracellular matrix metalloproteinase inducer, can function as a key mediator of inflammatory and immune responses. CD147 expression is increased in the brain after cerebral ischemia, but its role in the pathogenesis of ischemic stroke remains unknown. In this study, we show that CD147 acts as a key player in ischemic stroke by driving thrombotic and inflammatory responses...
November 7, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/29114077/the-ubiquitin-e3-ligase-traf6-exacerbates-ischemic-stroke-by-ubiquitinating-and-activating-rac1
#20
Tao Li, Juan-Juan Qin, Xia Yang, Yan-Xiao Ji, Fangliang Guo, Wen-Lin Cheng, Xiaolin Wu, Fu-Han Gong, Ying Hong, Xue-Yong Zhu, Jun Gong, Zhihua Wang, Zan Huang, Zhi-Gang She, Hongliang Li
Stroke is one of the leading causes of morbidity and mortality worldwide. Inflammation, oxidative stress, apoptosis, and excitotoxicity contribute to neuronal death during ischemic stroke; however, the mechanisms underlying these complicated pathophysiological processes remain to be fully elucidated. Here, we found that the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6) was markedly increased after cerebral ischemia/reperfusion (I/R) in mice. TRAF6 ablation in male mice decreased the infarct volume and neurological deficit scores, and decreased pro-inflammatory signaling, oxidative stress and neuronal death after cerebral I/R, whereas transgenic overexpression of TRAF6 in male mice exhibited opposite effects...
November 7, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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