• Middle cerebral artery (MCA) occlusion is achieved in this model by injecting particles like blood clots (thrombembolic MCAO) or artificial spheres into the carotid artery of animals as an animal model of ischemic stroke. (wikipedia.org)
  • However, the quality of MCAO - and thus the volume of brain infarcts - is very variable, a fact which is further aggravated by a certain rate of spontaneous lysis of injected blood clots. (wikipedia.org)
  • The purpose of this study is to establish and validate an animal model for research in the recovery and sequela stages of brain ischemia by testing brain infarction and sensorimotor function after middle cerebral artery occlusion/reperfusion (MCAO/R) after 1-90 days in rats. (jove.com)
  • The model used in this study was established by middle cerebral artery occlusion (MCAO) and reperfusion. (biomedcentral.com)
  • Transient middle cerebral artery occlusion (MCAO) is induced in both wild-type and Mcpip1 -/- mice for 2 hours of occlusion periods followed by reperfusion for 24 or 48 hours. (preprints.org)
  • Absence of MCPIP1 leaded to significant increase in FITC-dextran leakage in peri-infarct brain, significant upregulation of MMP-9, MMP-3 and reduced levels of tight junction components, claudin-5 and ZO-1 in the brain after MCAO. (preprints.org)
  • METHODS: Ischemia was induced by the intraluminal suture method, for 60 min of middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. (starrlifesciences.com)
  • RESULTS: Compared with wild type littermates, infarct volume was decreased by 22.3% in β2AR knockout mice (39.7 ± 10.7 mm3 vs 51.0 ± 11.4 mm3, n = 10/group, P = 0.034) after 60 min of MCAO followed by 24 h reperfusion. (starrlifesciences.com)
  • CONCLUSION: Brain injury is reduced and neurological outcome improved after MCAO in mice lacking the β2AR, or in wild type mice pretreated with a selective β2AR antagonist. (starrlifesciences.com)
  • We used middle cerebral artery occlusion (MCAO) to make the CIRI model in rats and monitored region cerebral blood flow (rCBF) to ensure that blood flow was blocked and recanalized. (sciencegate.app)
  • Various concentrations of SUF, especially 5, 10 and 25 μg/kg of SUF, all alleviated the infarct size, neurological function and brain edema of MCAO rats. (sciencegate.app)
  • SUF pretreatment effectively improved the neurological function and cerebral infarction of MCAO rats, inhibited excessive inflammation in rats, protected the BBB, and inhibited cell apoptosis in brain tissue. (sciencegate.app)
  • Sixty rats were subjected to a transient middle cerebral artery occlusion (MCAO). (linc-stg.eu)
  • Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. (biomedcentral.com)
  • Therefore, our data support the hypothesis that EA could exert its anti-inflammatory effect via inhibiting the astroglial and microglial/macrophage P2 purinoceptors (P2X7R and P2Y1R)-mediated neuroinflammation after MCAO/R injury. (biomedcentral.com)
  • Here, we sought to discover whether one effect of fenofibrate might include the suppression of the acute phase response (APR) following brain injury.A 1-h intraluminal thread middle cerebral artery occlusion (MCAO) model followed by a 6-h reperfusion was performed in C57/BL6 mice. (ox.ac.uk)
  • Quantitative reverse transcriptase-polymerase chain reaction was then used to measure hepatic expression of chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine ligand 10 (CXCL10) and serum amyloid A-1 (SAA-1), and immunohistochemical analysis was used to quantify brain and hepatic neutrophil infiltration following stroke.The MCAO and sham surgery induced the expression of all three acute phase reactants. (ox.ac.uk)
  • Water electrolysis-derived hydrogen inhalation had neuroprotective effects on cerebral ischemia/reperfusion injury in rats with the effect of suppressing oxidative stress and inflammation, and it is a possible new hydrogen resource to electrolyze water at the bedside clinically. (molecularhydrogenstudies.com)
  • Abstract BACKGROUND: Several β-adrenergic receptor (βAR) antagonists have been shown to have neuroprotective effects against cerebral ischemia. (starrlifesciences.com)
  • Celastrol is a bioactive compound that has been found to exhibit neuroprotective effects in cerebral ischemia, while whether it can protect against cerebral I/R injury by regulating glycolysis remains unclear. (sciencegate.app)
  • NRP-1 can produce neuroprotective effects against I/R injury to the brain by activating the Wnt/β-catenin signaling pathway and promoting mitochondrial structural repair and functional recovery, which may serve as a promising candidate target in treating ischemic stroke. (biomedcentral.com)
  • 13. Zhang W, Miao Y, Zhou S, Jiang J, Luo Q, Qiu Y. Neuroprotective effects of ischemic postconditioning on global brain ischemia in rats through upregulation of hippocampal glutamine synthetase. (ac.ir)
  • In C57Bl/6 (wildtype, WT), hcn2 +/+ and hcn2 -/- mice we used an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of HCN2 in stroke formation. (biomedcentral.com)
  • Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice. (scienceopen.com)
  • Adeno-associated viral (AAV)-NRP-1 was stereotaxically inoculated into the cortex and ipsilateral striatum posterior of adult male Sprague-Dawley (SD) rats before a 90-min transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion. (biomedcentral.com)
  • Neurological score was determined at 24 h reperfusion and infarct size was determined by cresyl violet or 2,3,5-triphenyltetrazolium chloride staining. (starrlifesciences.com)
  • Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (biomedcentral.com)
  • After cerebral hypoxia-ischemia, endogenously produced brain lactate is largely increased, and the exogenous administration of more lactate can decrease lesion size and ameliorate the neurological outcome. (edu.sa)
  • This treatment reduced the volume of brain lesion and the neurological deficit, as evaluated 1 and 7 days later. (csic.es)
  • Repeated treatments with Catalpol reduced neurological deficits and significantly improved angiogenesis, while significantly increasing brain levels of EPO and VEGF without worsening BBB edema. (researchgate.net)
  • Neurological assessment was performed, brain tissue damage was quantified, and NLRP1 and NLRP3 inflammasome protein levels were evaluated. (scienceopen.com)
  • Subsequently, brain infarct size, brain edema and Evans Blue dye extravasations were measured and neurological deficits were scored. (nih.gov)
  • Induction of cerebral ischemia in the control group produced severe neurological sensorimotor deficits in conjunction with considerable cerebral infarctions. (ac.ir)
  • Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)
  • This study aimed to investigate whether resuscitation after a hemorrhagic shock (HS) and/or mild cerebral ischemia caused by a unilateral common carotid artery occlusion (UCCAO) can cause brain injury and concomitant neurological dysfunction, and explore the potential mechanisms. (medsci.org)
  • An UCCAO caused a slight cerebral ischemia (cerebral blood flow [CBF] 70%) without hypotension (MABP 85 mmHg), systemic inflammation, multiple organs injuries, or neurological injury. (medsci.org)
  • However, combined an UCCAO and an HS caused a severe cerebral ischemia (18% of the original CBF levels), a moderate hypotension (MABP downed to 17 mmHg), systemic inflammation, peripheral organs damage, and neurological injury, which can be attenuated by whole body cooling. (medsci.org)
  • A resuscitation from an HS regards as a reperfusion insult which may induce neurological injury in patients with an UCCAO disease. (medsci.org)
  • However, it is not known whether resuscitation after a [ 10 - 12 ] HS can cause cerebral injury and concomitant neurological dysfunction, and its potential mechanisms. (medsci.org)
  • Rats were subjected to 100 mins middle cerebral artery occlusion followed by assessment of infarct volume, neurological score, mitochondrial function, and levels of oxidative stress at 24 h reperfusion. (starrlifesciences.com)
  • Here we characterized the effect of intraspinal grafting of clinical grade human fetal spinal cord-derived neural stem cells (HSSC) on the recovery of neurological function in a rat model of acute lumbar (L3) compression injury. (biomedcentral.com)
  • The results showed that puerarin derivative P1-EA and P2-EA were resulting in an increased lipophilicity that enabled the derivatives to pass more efficiently through the blood-brain barrier, thus, improving the protective effects against cerebral ischemia/reperfusion injury. (hindawi.com)
  • Studies have shown that puerarin reduced cerebral edema in rats with cerebral ischemia-reperfusion injury, removed lipid peroxidation products, enhanced antioxidant capacity, improved antioxidant activity of the brain tissue, and reduced the degree of focal cerebral ischemic injury [ 2 - 4 ]. (hindawi.com)
  • They do not have a Circle of Willis and stroke can be induced by common carotid artery occlusion alone. (wikipedia.org)
  • Middle Cerebral Artery Occlusion Allowing Reperfusion via Common Carotid Artery Repair in Mice JOVE-JOURNAL OF VISUALIZED EXPERIMENTS. (nottingham.ac.uk)
  • The most common causes of arterial occlusion involving the major cerebral arteries are (1) emboli, most commonly arising from atherosclerotic arterial narrowing at the bifurcation of the common carotid artery, from cardiac sources, or from atheroma in the aortic arch and (2) a combination of atherosclerotic stenosis and superimposed thrombosis. (medscape.com)
  • When injecting spheres into the cerebral circulation, their size determines the pattern of brain infarction: Macrospheres (300-400 µm) induce infarcts similar to those achieved by occlusion of the proximal MCA [5], whereas microsphere (~ 50 µm) injection results in distal, diffuse embolism [6]. (wikipedia.org)
  • Mannitol infusion performed immediately after restitution of blood flow following temporary cerebral ischemia remarkably reduced the size of the cerebral cortical focal infarction by decreasing the swelling of the end‐feet, thus preventing the microvascular compression and stasis and thereby microvasculogenic secondary focal cerebral ischemia. (nii.ac.jp)
  • RAT"}]}, "item_6_textarea_68": {"attribute_name": "wosonly abstract", "attribute_value_mlt": [{"subitem_textarea_value": "Previously we found that, after temporary cerebral ischemia, microvasculogenic secondary focal cerebral cortical ischemia occurred, caused by microvascular obstruction due to compression by swollen astrocytic end-feet, resulting in focal infarction. (nii.ac.jp)
  • Cerebral infarction (cerebral infarction), also known as acute ischemic stroke (acute cerebral ischemic stroke), refers to the necrosis of the localized brain tissue caused by cerebral blood circulation disorder, ischemia and hypoxia. (crimsonpublishers.com)
  • Ischemia reperfusion injury is one of the important injury factors in the process of cerebral infarction, and its pathological process is very complicated. (crimsonpublishers.com)
  • In the treatment of acute cerebral infarction, it is possible to remove the arterial thrombosis as early as possible, make the occlusion of the cerebral artery repasses, restore or improve the blood supply of the infarct area, prevent the ischemia reperfusion injury, save the ischemic penumbra, prevent the irreversible injury of ischemic brain tissue, and reduce the mortality and the rate of disability. (crimsonpublishers.com)
  • Factors that modify the extent of infarction include the speed of occlusion and systemic blood pressure. (medscape.com)
  • When cerebral ischemia-reperfusion injury happened in patients, multiple pathological processes occur, such as leukocyte infiltration, platelet, and complement activation, which would result in cognitive dysfunction and inflammation. (hindawi.com)
  • Cerebral ischaemia is caused by middle cerebral artery occlusion, which leads to some brain tissue damage, accompanied by inflammation and immune response [ 2 ]. (biomedcentral.com)
  • Biochemically, hydrogen inhalation decreased brain caspase-3, 3-nitrotyrosine and 8-hydroxy-2-deoxyguanosine-positive cells and inflammation factors concentration. (molecularhydrogenstudies.com)
  • An HS caused a moderate cerebral ischemia (52% of the original CBF levels), a moderate hypotension (MABP downed to 22 mmHg), systemic inflammation, and peripheral organs injuries. (medsci.org)
  • However, the direct effects and features of systemic inflammation on brain injury, especially comparing between ischaemic and haemorrhagic stroke, are still obscure. (bmj.com)
  • Furthermore, we demonstrated that PT enhanced brain inflammation and aggravated stroke severity in middle cerebral artery occlusion mouse model. (bmj.com)
  • Roles of Peroxisome Proliferator-Activated Receptor Gamma on Brain and Peripheral Inflammation. (nih.gov)
  • We used β2AR knockout mice and a β2selective antagonist to test the effect of loss of β2ARs on outcome from transient focal cerebral ischemia. (starrlifesciences.com)
  • After cerebral ischemia, total levels of Hsp72 and the number of Hsp72 immunopositive cells were greater in mice lacking β2 AR. (starrlifesciences.com)
  • Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice? (biomedcentral.com)
  • After 60 min of tMCAO induction in WT mice, we collected tissue samples at 6, 12, and 24 h after reperfusion. (biomedcentral.com)
  • To test whether HCAR1 plays a role in lactate-induced neuroprotection, we injected the agonists 3-chloro-5-hydroxybenzoic acid and 3,5-dihydroxybenzoic acid into mice subjected to 30-min middle cerebral artery occlusion. (edu.sa)
  • Primary cortical neurons were subjected to glucose deprivation (GD), oxygen-glucose deprivation (OGD) or simulated ischemia-reperfusion (I/R). Ischemic stroke was induced in C57BL/6J mice by middle cerebral artery occlusion, followed by reperfusion. (scienceopen.com)
  • Similarly, levels of NLRP1 and NLRP3 inflammasome proteins, IL-1 β and IL-18 were elevated in ipsilateral brain tissues of cerebral I/R mice and stroke patients. (scienceopen.com)
  • Male C57Bl/6 mice were subjected to focal cerebral ischemia and periods of reperfusion (0, 8 and 24 h). (biomedcentral.com)
  • Live cell morphology and process activity were measured from movies acquired in acute brain slices from GFP-CX3CR1 transgenic mice after IS and 24-h reperfusion. (biomedcentral.com)
  • We also found that female mice sustained smaller infarcts than males three months post- ischemia . (nih.gov)
  • [ 1 ] A recent hypothesis to explain the migraine-stroke association, based on experimental data obtained in mice expressing familial hemiplegic migraine type 1 mutations, is that the cerebral hyperexcitability phenotype associated with migraine might sensitize brain tissue to ischemia. (medscape.com)
  • The area of injury is typically concentrated in periventricular regions of the brain, especially cortical and hippocampal areas. (wikipedia.org)
  • Ischemia-like conditions increased the levels of NLRP1 and NLRP3 inflammasome proteins, and IL-1 β and IL-18, in primary cortical neurons. (scienceopen.com)
  • Caspase-1 inhibitor treatment protected cultured cortical neurons and brain cells in vivo in experimental stroke models. (scienceopen.com)
  • Lentivirus (LV)-NRP-1 was transfected into rat primary cortical neuronal cultures before a 2-h oxygen-glucose deprivation and reoxygenation (OGD/R) injury to neurons. (biomedcentral.com)
  • Microglia were both hyper- and de-ramified in striatal and cortical brain regions (respectively) after 60 min of focal cerebral ischemia. (biomedcentral.com)
  • Compared to the oxygen-glucose deprivation/reperfusion group, the protein and mRNA expressions of p-JNK, Bax, cleaved Caspase3 was decreased significantly. (archive.org)
  • They are divided into techniques including reperfusion of the ischemic tissue (transient focal cerebral ischemia) and those without reperfusion (permanent focal cerebral ischemia). (wikipedia.org)
  • Twenty-two hours after re-perfusion the rats were assessed for neurobehavioral deficit, infarct volume, histological changes, and malondialdehyde, superoxide dismutase (SOD), Bcl-2 and NF-?B levels in brain tissue. (edu.au)
  • Safflower injection can correct the imbalance of thromboxane (TXA2) HJNKM / prostacyclin (PGI2) and abnormal changes of the ultrastructure of brain tissue in circulating blood after cerebral ischemia-reperfusion, and reduce the injury of cerebral ischemia reperfusion. (crimsonpublishers.com)
  • The depletion of oxygen or glucose in ischemic brain tissue sets off a series of interrelated events that result in neurodegeneration. (biomedcentral.com)
  • We used ELISA and RT-PCR to detect the expression of inflammatory factors in rat serum and brain tissue. (sciencegate.app)
  • Multi-protein complexes called inflammasomes have recently been identified and shown to contribute to cell death in tissue injury. (scienceopen.com)
  • NLRP1 and NLRP3 inflammasome components were also analyzed in postmortem brain tissue samples from stroke patients. (scienceopen.com)
  • The damage from ICH includes the primary tissue injury due to the mechanical effects of the haemorrhage and also the development of perihaematomal oedema (PHO), which induces a severe secondary injury and/or destruction of the adjacent tissue, in addition to an impairment in the integrity of the blood-brain barrier (BBB). (bmj.com)
  • The extension of the necrotic core into the penumbra is influenced by additional factors such as regional differences in the composition of brain tissue, the vulnerability of different cell types to ischemia, residual tissue perfusion and additional events such as reperfusion [ 2 - 4 ]. (biomedcentral.com)
  • Central nervous system (CNS) damage may occur because of hypoxemia sustained during the drowning episode (primary injury) or may result from arrhythmias, ongoing pulmonary injury, reperfusion injury, or multiorgan dysfunction (secondary injury), particularly with prolonged tissue hypoxia. (medscape.com)
  • Cerebral hyperexcitability in migraine experiencers might sensitize brain tissue to ischemia. (medscape.com)
  • Along with the observation that migraine mutants had an elevated minimum cerebral blood flow threshold required for tissue survival and developed larger infarcts, these findings directly support the hypothesis that brain tissue in migraineurs is more susceptible to ischemic injury. (medscape.com)
  • Based on these premises, taking advantage of the reliability of computed tomography perfusion (CTP) imaging in the estimation of cerebral tissue viability in both clinical and research settings, [ 4 ] we conducted a case-control study comparing CTP maps of migraineurs and nonmigraineurs patients with acute ischemic stroke aimed at investigating whether a personal history of migraine is associated with vulnerability to brain ischemia. (medscape.com)
  • Animal models of ischemic stroke are procedures inducing cerebral ischemia. (wikipedia.org)
  • However, they are less immediately relevant to human stroke than the focal stroke models, because global ischemia is not a common feature of human stroke. (wikipedia.org)
  • Exogenous endothelin-1 can also be used to induce stroke and cell death after sustained vasoconstriction with reperfusion. (wikipedia.org)
  • Pre-stroke surgery is not beneficial to normotensive rats undergoing sixty minutes of transient focal cerebral ischemia PLOS ONE. (nottingham.ac.uk)
  • I am particularly interested in developing novel MRI methodologies for examining brain function, investigating the role of sex and steroid hormones in ischaemic stroke/cognitive decline and increasing the translational relevance of experimental models of CNS injury and disease. (nottingham.ac.uk)
  • We selected stroke‐positive animals during the first 10 min after left carotid occlusion performed twice with a 5‐h interval, and allocated them into four groups: sham‐operated control, no‐treatment, mannitol‐infusion, and saline‐infusion groups. (nii.ac.jp)
  • According to the theory of TCM, cerebral ischaemia, which is also called stroke, can be induced by hyperactivity of liver Yang, disordered diet, stagnation of blood, etc. (biomedcentral.com)
  • The role of the anti-inflammatory protein, monocyte chemotactic protein-induced protein 1 (MCPIP1) plays in the injury of BBB in stroke has not yet been reported. (preprints.org)
  • Occlusion of single penetrating branches of the middle and anterior cerebral arteries that supply the deep white and gray matter produce the lacunar type of stroke. (medscape.com)
  • Ischemic stroke occurs due to an interruption of blood supply to corresponding areas of the brain, initiating an ischemic cascade. (biomedcentral.com)
  • Stroke is a brain system disease with a high fatality rate and disability rate. (sciencegate.app)
  • Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. (sciencegate.app)
  • Reperfusion is the best way to protect the brain against ischemic injury and, up to now, thrombolysis with rt-PA is the only approved treatment for ischemic stroke that has shown efficacy in large clinical trials worldwide. (csic.es)
  • Emerging evidences indicate that systemic inflammatory cascades after stroke contribute to brain damage. (bmj.com)
  • The neurodeficits, stroke lesion, immune response and blood-brain barrier (BBB) destruction were assessed. (bmj.com)
  • Conclusions Our results suggest that PT increases inflammatory response that exacerbates brain injury after ICH or ischaemic stroke in mouse model. (bmj.com)
  • 1 2 At present, although progress has been made in understanding the molecular and cellular pathways leading to brain injury after stroke, the current clinical treatments remain poorly effective. (bmj.com)
  • Although ideally positioned for immediate response to ischemic stroke (IS) and reperfusion, their progressive morphological transformation into activated cells has not been quantified. (biomedcentral.com)
  • CD11b expression, but not iNOS expression, was increased in regions of hyper- and de-ramified microglia during the course of ischemic stroke and 24 h of reperfusion. (biomedcentral.com)
  • 11. Dinapoli VA, Rosen CL, Nagamine T, Crocco T. Selective MCA occlusion: a precise embolic stroke model. (ac.ir)
  • 21. Zhao H. Ischemic postconditioning as a novel avenue to protect against brain injury after stroke. (ac.ir)
  • Aim of this project is to characterize the entire imaging spectrum of brain health in stroke and TIA patients in collaboration with Department of Neurology's* large population based study. (uc.edu)
  • Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. (medscape.com)
  • Multicenter cohort study of patients with acute ischemic stroke who underwent a brain computed tomography perfusion and were scheduled to undergo reperfusion therapy. (medscape.com)
  • Migraine is likely to increase individual vulnerability to ischemic stroke during the process of acute brain ischemia and might represent, therefore, a potential new therapeutic target against occurrence and progression of the ischemic damage. (medscape.com)
  • CR-6 protects the ischemic brain against reperfusion injury. (csic.es)
  • Our previous studies have demonstrated that EA protects cerebral neural cells against inflammatory injury after cerebral ischemia, which appears at 24 h to 14 days after treatment. (biomedcentral.com)
  • 4. Ren C, Gao X, Niu G, Yan Z, Chen X, Zhao H. Delayed postconditioning protects against focal ischemic brain injury in rats. (ac.ir)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • rat model by middle cerebral artery occlusion. (archive.org)
  • Sprague-Dawley rats were used as experimental animals, and middle cerebral artery occlusion was used to make cerebral ischemia/reperfusion model. (molecularhydrogenstudies.com)
  • Two and eight hours after focal brain ischemia (90 min-occlusion of the middle cerebral artery), rats received oral administration of the antioxidant CR-6, a synthetic derivative of vitamin E that can scavenge oxygen and nitrogen reactive species. (csic.es)
  • i.p) or vehicle administered 24 hours after permanent middle cerebral artery occlusion (pMCAO) on behavior, angiogenesis, ultra-structural integrity of brain capillary endothelial cells, and expression of EPO and VEGF were assessed. (researchgate.net)
  • Two hours after the last dose, serum lipid levels were determined and then the rats were subjected to 60 min of middle cerebral artery occlusion followed by 24 h of reperfusion. (nih.gov)
  • Transient focal cerebral ischemia (90 min) was induced by occlusion of the left middle cerebral artery that followed by 24 h reperfusion periods. (ac.ir)
  • SUMO2/3 is associated with ubiquitinated protein aggregates in the mouse neocortex after middle cerebral artery occlusion. (cornell.edu)
  • 14. Bederson JB, Pitts LH, Tsuji M, Nishimura MC, Davis RL, Bartkowski H. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. (ac.ir)
  • Mechanisms of ischemia resulting from internal carotid artery occlusion are, most commonly, artery-to-artery embolism or propagating thrombus and perfusion failure from distal insufficiency. (medscape.com)
  • Often, ischemia in the distribution of the ophthalmic artery is transient in the setting of symptomatic internal carotid artery occlusion (ie, transient monocular blindness, occurring in approximately 25% of patients), but central retinal artery ischemia is relatively uncommon, presumably because of the efficient collateral supply. (medscape.com)
  • Brain glutamate levels were determined by in vivo MR spectroscopy (MRS) during artery occlusion (80 min) and reperfusion (180 min). (linc-stg.eu)
  • The original phenolic hydroxyl in the puerarin molecules was substituted in order to change the blood-brain barrier permeability and thus enhance the efficacy for preventing cerebral ischemia/reperfusion injury. (hindawi.com)
  • However, the development of new drugs to treat central nervous system disorders is limited by many factors, primarily, delivery to the brain through the blood-brain barrier. (hindawi.com)
  • In addition, we tested the anticerebral ischemia-reperfusion injury activity of these puerarin derivatives in order to determine their permeability through the blood-brain barrier and pharmacological activity. (hindawi.com)
  • Focal cerebral ischemia can lead to blood-brain barrier (BBB) breakdown, which is implicated in neuroinflammation and elevation of matrix metalloproteinases (MMPs). (preprints.org)
  • Our data demonstrate that absence of MCPIP1 exacerbates ischemia-induced blood-brain barrier disruption by enhancing the expression of matrix metalloproteinases and degradation of tight junction proteins. (preprints.org)
  • In addition, we detected the expression of metalloproteinase (MMP) 2, MMP9 and collagen IV in brain tissues and performed Evans blue (EB) assay to determine the permeability of the blood-brain barrier (BBB). (sciencegate.app)
  • it attenuated blood-brain barrier damage and oedema, leukocyte infiltration, and expression of a set of proinflammatory molecules. (csic.es)
  • However, it displays poor blood-brain barrier permeability leading to some ambiguity over its mechanism of action. (ox.ac.uk)
  • Overexpression of Hsp75 was achieved in rat brain by DNA transfection, and expression was observed in both astrocytes and neurons. (starrlifesciences.com)
  • Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
  • Magnetic resonance imaging volume reconstruction and immunofluorescence analysis of grafted cell survival showed near complete injury-cavity-filling by grafted cells and development of putative GABA-ergic synapses between grafted and host neurons. (biomedcentral.com)
  • A separate group of experimental treatment modalities is aimed at improving the local neurotrophic activity at and around the injury epicenter with the primary goal of increasing the survival of partially injured axons and/or neurons. (biomedcentral.com)
  • Protective effect of rGOT1 supplemented with oxaloacetate at 7 days persists even when treatment was delayed until at least 2 h after onset of ischemia. (linc-stg.eu)
  • Isosteviol has been demonstrated to have protective effects against ischemia-reperfusion (IR) injury in the rat heart and the current study was undertaken to determine whether it is also effective in preventing IR injury in the brain. (edu.au)
  • Thus, how can rhubarb anthraquinone glycosides (RAGs) exert protective effects on the brain? (biomedcentral.com)
  • Our results suggest that the protective effects of lactate after hypoxia-ischemia come rather from the metabolic effects of lactate than its signaling through HCAR1. (edu.sa)
  • Human recombinant glutamate oxaloacetate transaminase 1 (GOT1) supplemented with oxaloacetate induces a protective effect after cerebral ischemia. (linc-stg.eu)
  • We recently reported that neonatal ischemia induces microglia/macrophage activation three days post- ischemia . (nih.gov)
  • Publisher Correction: Cerebral ischemia induces the aggregation of proteins linked to neurodegenerative diseases. (cornell.edu)
  • In this study, we first constructed Oxygen and glucose deprivation/reoxygenation (OGD/R) injury model of PC12 cells, we found that the expression of LncRNA AK139328 in model cells was significantly increased through RT-qPCR. (sciencegate.app)
  • The patterns of arterial occlusion are different in African Americans and Asians than in whites. (medscape.com)
  • Thereby, the acidified milieu after arterial occlusion most probably influences the activity of acid-sensing ion channels as well as the cell membrane potential. (biomedcentral.com)
  • Hydroxycarboxylic Acid Receptor 1 and Neuroprotection in a Mouse Model of Cerebral Ischemia-Reperfusion. (edu.sa)
  • Dive into the research topics of 'Hydroxycarboxylic Acid Receptor 1 and Neuroprotection in a Mouse Model of Cerebral Ischemia-Reperfusion. (edu.sa)
  • Therefore, over the past several years, research has been directed to limit the brain lesions produced by acute ischemia (neuroprotection) and to increase the recovery, plasticity and neuroregenerative processes that complement rehabilitation and enhance the possibility of recovery and return to normal functions (neurorepair). (mdpi.com)
  • These occlusions account for as many as 20% of ischemic strokes. (medscape.com)
  • The IMPROVE Guidelines (Ischaemia Models: Procedural Refinements Of in Vivo Experiments). (nottingham.ac.uk)
  • The in vivo administration of HCAR1 agonists at reperfusion did not appear to exert any relevant protective effect as seen with lactate administration. (edu.sa)
  • Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
  • abstract = "Lactate is an intriguing molecule with emerging physiological roles in the brain. (edu.sa)
  • Abstract Blood glutamate scavenging is a novel and attractive protecting strategy to reduce the excitotoxic effect of extracellular glutamate released during ischemic brain injury. (linc-stg.eu)
  • Vascular dementia (VaD) is characterized by a decline in brain function resulting in a cognitive impairment syndrome that is caused by various cerebrovascular diseases such as ischemic, hemorrhagic, chronic, and polar hypoxic cerebrovascular diseases. (hindawi.com)
  • If so, the infusion of mannitol might improve the results of vascular reperfusion therapy. (nii.ac.jp)
  • REBOA procedures carrying life-threatening risks such as arterial access complications, organ ischemia, vascular trauma, and time loss ( 2 ) should be critically evaluated in addition to resuscitative laparotomy, thoracotomy with aortic cross-clamping, or manual aortic compression. (frontiersin.org)
  • Iatrogenic vascular injury is an unusual (0.02-0.06%) fatal complication of orthopedic or neurosurgical lumbar-disk procedures ( 3 ) demanding immediate availability of a trained multidisciplinary team of emergency specialists and vascular and endovascular surgeons. (frontiersin.org)
  • Early reperfusion strategies remain the treatment of choice but can initiate and augment an inflammatory response causing secondary brain damage. (scienceopen.com)
  • It is well-documented that extracellular ATP triggers surrounding glial purinergic receptors signaling pathway and pro-inflammatory cytokines release to aggravate neural injury in cerebral ischemia [ 8 , 9 ]. (biomedcentral.com)
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
  • We also found promoted leucocyte infiltration and inflammatory cytokine release into the brain after PT treatment. (bmj.com)
  • Although pretreatment with RHE plays an important role in the generation of tolerance against cerebral I/R injury, further studies are needed to clarify the mechanism of the ischemic tolerance. (nih.gov)
  • The role of PPAR activation during the systemic response to brain injury. (ox.ac.uk)
  • This case report describes resuscitative endovascular balloon occlusion (REBOA) of the aorta in a patient with life-threatening iatrogenic bleeding of the right common iliac artery during elective dorsal lumbar spine surgery. (frontiersin.org)
  • Resuscitative endovascular balloon occlusion of the aorta is an emergency procedure to control life-threatening hemorrhage. (frontiersin.org)
  • Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an emergency procedure for temporary intra-aortic balloon occlusion being increasingly reported and published since its inauguration by Hughes ( 1 ). (frontiersin.org)
  • Then the aorta is cross-clamped and the heart is stopped by injection of a cardioplegic solution (crystalloid or more commonly blood-based) that also contains substances that help myocardial cells tolerate ischemia and reperfusion. (msdmanuals.com)
  • Depending upon the degree of hypoxemia and resultant acidotic change in acid-base balance, the person may develop myocardial dysfunction and electrical instability, cardiac arrest, and CNS ischemia. (medscape.com)
  • These results suggested that catalpol might contribute to infarcted-brain angiogenesis and ameliorate the edema of brain capillary endothelial cells (BCECs) by upregulating VEGF and EPO coordinately. (researchgate.net)
  • The mouse model of cerebral artery ischemia/reperfusion injury was established to test the anticerebral ischemia-reperfusion injury activity of the puerarin derivatives. (hindawi.com)
  • The assays of the water maze, Y maze, brain cortex Ca 2+ -Mg 2+ -ATP enzyme, and iNOS enzyme activity were performed in this mouse model. (hindawi.com)
  • This approach is useful to study hypoxic ischemia in the developing brain, since newborn rat pups are utilized in this model. (wikipedia.org)
  • This model creates a unilateral infarct in the hemisphere ipsilateral to the ligation, since the hypoxia alone is subthreshold for injury at this age. (wikipedia.org)
  • This study uses an established animal model to research the recovery and the sequelae stages of brain ischemia. (jove.com)
  • The objectives of this study were to define the temporal and spatial infiltration of immune cell populations and their activation patterns in a murine cerebral ischemia-reperfusion injury model. (scienceopen.com)
  • 18. Wang CX, Yang T, Shuaib A. An improved version of embolic model of brain ischemic injury in the rat. (ac.ir)
  • The three treatments tested induced a reduction in serum and brain glutamate levels, resulting in a reduction in infarct volume and sensorimotor deficit. (linc-stg.eu)
  • A 14-day fenofibrate pre-treatment decreased reactant production, infarct volume, and neutrophil recruitment to the brain and liver, which is a hallmark of the APR.The data highlight a novel mechanism of action for fenofibrate and lend further evidence towards the promotion of its use as a prophylactic therapy in patients at risk of cerebral ischaemia. (ox.ac.uk)
  • The abundance and diversity of the intestinal flora in rats decreased after cerebral ischaemia - reperfusion injury (CIRI). (biomedcentral.com)
  • Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that the ischemic injury of brain leads to the injury of brain cells, and ischemic injury is further aggravated after the recovery of blood reperfusion. (sciencegate.app)
  • Nissl staining and NeuN staining were utilized to observe the numbers and structures of neuron cells, and the pathological changes in the brain tissues were examined by hematoxylin-eosin staining. (archive.org)
  • A wealth of studies now confirm that PQQ's cell-signaling activity translates into substantial protection against degenerative and age-related conditions, such as mitochondrial dysfunction, 1 heart degeneration, 18-20 brain injury, and cognitive decline. (lifeextension.com)
  • In case of ongoing CPR, we recommend surgical groin incision, open puncture of the pulseless common femoral artery, and aortic balloon inflation in REBOA zone I. Hereby, fast access and CPR optimization for heart and brain perfusion are maintained. (frontiersin.org)
  • I lead a basic neuroscience research group which is primarily interested in investigating mechanims of injury following CNS injury and disease. (nottingham.ac.uk)
  • It has beneficial effects in animal models of acute brain injuries and traumatic brain injury or subarachnoid hemorrhage patients. (edu.sa)
  • In former studies the expression of two different two-pore domain potassium (K 2P ) channels (TASK1, TREK1) were shown to ameliorate neuronal damage due to cerebral ischemia. (biomedcentral.com)
  • However, in various settings global ischemia is also relevant, e.g. in global anoxic brain damage due to cardiac arrest. (wikipedia.org)
  • Damage to Myelin and Oligodendrocytes: A Role in Chronic Outcomes Following Traumatic Brain Injury? (mdpi.com)
  • Peri-acute intraspinal grafting of HSSC can represent an effective therapy which ameliorates motor and sensory deficits after traumatic spinal cord injury. (biomedcentral.com)
  • This treatment could benefit a subset of patients receiving rt-PA that may be at risk of developing secondary complications due to reperfusion. (csic.es)