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Reperfusion InjuryMyocardial Reperfusion InjuryIschemiaReperfusionNeuronsMyocardial IschemiaMyocardial ReperfusionBrain IschemiaIschemic PreconditioningRats, Sprague-DawleyRats, WistarNeurons, AfferentIschemic Preconditioning, MyocardialMyocardiumDisease Models, AnimalTime FactorsMotor NeuronsMyocardial InfarctionIschemic PostconditioningCardiotonic AgentsWarm IschemiaMice, Inbred C57BLPeroxidaseNeuroprotective AgentsIschemic Attack, TransientBrainApoptosisCold IschemiaProtective AgentsHeartMalondialdehydeInfarction, Middle Cerebral ArteryMyocytes, CardiacOxidative StressMice, KnockoutCells, CulturedHippocampusPerfusionImmunohistochemistryNecrosisCoronary CirculationMitochondria, HeartAction PotentialsSpinal Cord IschemiaL-Lactate DehydrogenaseKidneyRandom AllocationCerebral CortexCreatine KinaseConstrictionCytoprotectionSuperoxide DismutaseGerbillinaeHemodynamicsMyocardial ContractionSignal TransductionReactive Oxygen SpeciesCell DeathAntioxidantsMice, TransgenicNitric OxideNeutrophil InfiltrationAnimals, NewbornModels, AnimalAnalysis of VarianceLiverDogsTioproninMyocardial StunningBlotting, WesternCerebral InfarctionHindlimbDopaminergic NeuronsEnzyme InhibitorsIn Situ Nick-End LabelingRNA, MessengerOrgan PreservationAspartate AminotransferasesCaspase 3CalciumRabbitsAcute Kidney InjuryFree Radical ScavengersCerebrovascular CirculationElectrophysiologyNerve Tissue ProteinsAlanine TransaminaseVentricular Function, LeftMicrocirculationDose-Response Relationship, DrugHydroxy AcidsDecanoic AcidsIntestinesPatch-Clamp TechniquesOrgan Preservation SolutionsSpinal CordHeme Oxygenase-1Heart Arrest, InducedMesenteric Artery, SuperiorCell Survival
CerebralHippocampalAlleviating ischemia reperfusion injuryGlobal ischemiaApoptosisOcclusionNeurological deficit scoreReactive oxygenMemory deficitsStrokeShown that neuronsAstrocytesOxygenInflammationHypoxia-ischemiaMicrogliaTissueReoxygenationPenumbraExtracellular pHOxidativeInjury InducedVivoInfarct volumeInducesThalamicPyramidalThalamocorticalNeurologicBrain slicesVitroAcuteMethodsNeuralGlialCatheterProtectsInflammatoryImmatureImpairmentExperimentalInhibitorDamageNLRP3Cell deathPrimary
Cerebral54
  • Global cerebral ischemia followed by reperfusion, which leads to extensive neuronal damage, particularly the neurons in the hippocampal CA1 region. (springer.com)
  • Apoptosis is one of the major mechanisms that lead to neuronal death after cerebral ischemia and reperfusion. (springer.com)
  • The neuroprotective effects of remifentanil preconditioning against cerebral ischemia/reperfusion injury have been recently reported. (springer.com)
  • Here we investigated whether remifentanil postconditioning exerts neuroprotective effects against global cerebral ischemia/reperfusion injury in rats and its potential mechanisms. (springer.com)
  • Global cerebral ischemia was performed via 10 min of four-vessel occlusion. (springer.com)
  • We found remifentanil postconditioning markedly improved the spatial learning and memory as well as attenuated neuronal apoptosis in hippocampus caused by cerebral ischemia/reperfusion injury. (springer.com)
  • The results suggest that remifentanil postconditioning exhibits neuroprotective effects against global cerebral ischemia/reperfusion injury in rats, and its mechanisms might involve inhibition of neuronal apoptosis through the PI3K pathway. (springer.com)
  • Liang HW, Qiu SF, Shen J et al (2008) Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus. (springer.com)
  • Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
  • Jeong S, Kim SJ, Jeong C et al (2012) Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats. (springer.com)
  • However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.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)
  • Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
  • Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)
  • 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)
  • 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)
  • Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice. (scienceopen.com)
  • METHODS: Vehicle (dimethyl sulfoxide), a GPER agonist (G-1, 30 mug/kg), or a GPER antagonist (G-15, 300 mug/kg) were administered alone or in combination to young or aged male mice, or young intact or ovariectomized female mice, 1 hour before or 3 hours after cerebral ischemia-reperfusion. (monash.edu)
  • The present study aimed to investigate the effects of changes in heat shock protein (HSP)90β expression and verify whether HSP90β regulates EAAT2 expression in a cerebral ischemia‑reperfusion injury model. (spandidos-publications.com)
  • A model of cerebral ischemia‑reperfusion was established using the MCAO method. (spandidos-publications.com)
  • These results suggested that HSP90β is involved in the process of cerebral ischemia‑reperfusion injury in rats and that inhibition of HSP90β expression increases EAAT2 levels, conferring a neuroprotective effect in MCAO model rats. (spandidos-publications.com)
  • When ischemic stroke occurs, cerebral ischemia and hypoxia cause the release of excessive excitatory amino acids, mainly glutamic acid and aspartic acid, which exert excitotoxic effects on the central nervous system. (spandidos-publications.com)
  • These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.com)
  • Reperfusion injury is distinct from cerebral hyperperfusion syndrome (sometimes called "Reperfusion syndrome"), a state of abnormal cerebral vasodilation. (wikipedia.org)
  • 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. (uni-wuerzburg.de)
  • Methods 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. (uni-wuerzburg.de)
  • Adoptive transfer of Sig-1R intact bone marrow-derived macrophages (BMDMs) to Sig-1R knockout mice restored the clearance activity of dead/dying neurons, reduced infarct area and neuroinflammation, and improved long-term functional recovery after cerebral ischemia. (thno.org)
  • However, the combined effect of prophylactic zinc administration and therapeutic taurine treatment on intrauterine ischemia- (IUI-) induced cerebral damage remains unknown. (hindawi.com)
  • These results collectively indicate the chronicity of oxidative stress and an inadequate antioxidant response after a cerebral hypoxia-ischemia event and have motivated the development of preventive and therapeutic approaches against oxidative stress. (hindawi.com)
  • Cerebral ischemia was induced for 2 hours. (edu.au)
  • Cerebral ischemia-reperfusion (IR) triggers lipid peroxidation and inflammation, which exacerbate injury. (biomedcentral.com)
  • Emerging data implicate both 5-LOX and FLAP in the disease process of cerebral ischemia [ 6 ]. (biomedcentral.com)
  • The contents of inflammasome proteins were gradually increased after cerebral ischemia/reperfusion (I/R). EA stimulus attenuated NLRP3 inflammasome mediated inflammatory reaction and regulated the balance between proinflammatory factors and anti-inflammatory cytokines. (biomedcentral.com)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
  • As an integrated platform for triggering inflammation, inflammasome contributes to the pathogenesis of initiating innate immune response after cerebral ischemia/reperfusion (I/R)(Ismael et al. (biomedcentral.com)
  • As part of the PENUMBRA SYSTEM, the Reperfusion Catheters and Separators are indicated for use in the revascularization of patients with acute ischemic stroke secondary to intracranial large vessel occlusive disease (within the internal carotid, middle cerebral - M1 and M2 segments, basilar, and vertebral arteries) within 8 hours of symptom onset. (penumbrainc.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)
  • 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, 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)
  • 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)
  • 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)
  • 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)
  • This study aimed to investigate the therapeutic potential of Ser on cognitive dysfunction induced by transient global cerebral ischemia/reperfusion (tGI/R) and its mechanism of action. (cjphysiology.org)
  • Global cerebral ischemia is associated with delayed neuronal death. (asahq.org)
  • Its effects were evaluated on neuronal cell death and outcome after global cerebral ischemia. (asahq.org)
  • Global cerebral ischemia was induced by cardiocirculatory arrest. (asahq.org)
  • We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100 mg/kg) once a day for 7 days before the induction of transient cerebral ischemia. (haritaki.club)
  • Objective: To investigate the effects of Zhongfeng capsule on the autophagy-related proteins expression in rats with cerebral ischemia/reperfusion injury (CI/ RI), and to explore its neural protection mechanisms of the decoction. (bvsalud.org)
  • Methods: Rat middle cerebral artery ischemia/reperfusion injury model (ischemia for 2 h, reperfusion for 24 h) was prepared by the improved line plug method. (bvsalud.org)
  • Hypoxaemic reperfusion ameliorates the histopathological changes in the pig brain after a severe global cerebral ischaemic insult. (jamanetwork.com)
  • Ischemic stroke is sudden neurologic deficits that result from focal cerebral ischemia associated with permanent brain infarction (eg, positive results on diffusion-weighted MRI). (msdmanuals.com)
  • Previous studies of global brain hypoxia ischemia have primarily focused on injury to the cerebral cortex and to the hippocampus. (cdc.gov)
Hippocampal3
  • Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling positive cells and expression of Bcl-2 and Bax in the hippocampal CA1 region were assessed after reperfusion. (springer.com)
  • Using primary hippocampal neurons from Stat5a/b knock-out mice we have recently shown that the presence of functional Stat5 is required for the trophic but not for the protective effect of EPO against glutamate-induced toxicity [ 9 ]. (biomedcentral.com)
  • Hyperoxic reperfusion after global ischemia decreases hippocampal energy metabolism. (jamanetwork.com)
Alleviating ischemia reperfusion injury1
Global ischemia2
  • Charron C, Messier C, Plamondon H (2008) Neuroprotection and functional recovery conferred by administration of kappa- and delta 1-opioid agonists in a rat model of global ischemia. (springer.com)
  • Optogenetic analysis of neuronal excitability during global ischemia reveals selective deficits in sensory processing following reperfusion in mouse cortex. (ulethbridge.ca)
Apoptosis6
Occlusion1
  • Within two minutes without blood flow (due to heart stoppage or blood vessel occlusion) neurons lack the energy to power the sodium/potassium pump. (benbest.com)
Neurological deficit score3
  • They were evaluated at 24 h after reperfusion for brain infarction, neurological deficit score, and the expression of 5-LOX. (biomedcentral.com)
  • The infarct size, neurological deficit score, TUNEL staining and the expression of proinflammatory factors or anti-inflammatory cytokines were evaluated at 72 h after reperfusion in the presence or absence of either α7nAChR antagonist (α-BGT) or agonist (PHA-543,613). (biomedcentral.com)
  • Results: Compared with the sham operation group, the body weight and protein expressions of p-PI3k and p-Akt in brain tissue of rats were decreased significantly in the model group, while the brain index, neurological deficit score, gene and protein expressions of Beclin1 and LC3 were increased markedly in the model group(P４0.05 or P４0.01). (bvsalud.org)
Reactive oxygen3
Memory deficits3
  • Morris water maze task was used to quantify spatial learning and memory deficits after reperfusion. (springer.com)
  • In the Morris water maze task, Terminalia chebula extract (TCE) treatment reversed scopolamine-induced learning and memory deficits in acquisition and retention. (haritaki.club)
  • Hypercholesterolemia in rats impairs the cholinergic system and leads to memory deficits. (uibk.ac.at)
Stroke14
  • Caspase-1 inhibitor treatment protected cultured cortical neurons and brain cells in vivo in experimental stroke models. (scienceopen.com)
  • IVIg treatment protected neurons in experimental stroke models by a mechanism involving suppression of NLRP1 and NLRP3 inflammasome activity. (scienceopen.com)
  • Our findings provide evidence that the NLRP1 and NLRP3 inflammasomes have a major role in neuronal cell death and behavioral deficits in stroke. (scienceopen.com)
  • We evaluated functional and histological end points of stroke outcome up to 72 hours after ischemia-reperfusion. (monash.edu)
  • An ischemic stroke consists of two related pathological injury processes: Primary ischemia-induced brain injury and secondary ischemia reperfusion injury ( 3 ). (spandidos-publications.com)
  • Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. (wikipedia.org)
  • Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice? (uni-wuerzburg.de)
  • Hypoxia and ischemia of the brain are key pathophysiological mechanisms of ischemic stroke ( 5 , 6 ). (frontiersin.org)
  • Adoptive transfer of Sig-1R intact macrophages to recipient Sig-1R knockout mice with tMCAO was developed to observe its effect on apoptotic neuron clearance and stroke outcomes. (thno.org)
  • Ischemia and reperfusion can cause serious brain damage in stroke or cardiac arrest. (benbest.com)
  • In this article I attempt to evaluate the nature & extent of ischemic & reperfusion injury -- primarily focused on the impact for cryonics (although certainly relevant to stroke and cardiac arrest). (benbest.com)
  • BACKGROUND: Astrocytes have been demonstrated to undergo conversion into functional neurons, presenting a promising approach for stroke treatment. (bvsalud.org)
  • RESULTS: In rats with ischemic stroke, miR-124-transduced glial cells exhibited positive staining for the immature neuron marker doublecortin (DCX) and the mature neuron marker NeuN after 4 weeks. (bvsalud.org)
  • CONCLUSIONS: The overexpression of miR-124 in astrocytes demonstrates significant potential for improving neurological deficits following ischemic stroke by inhibiting DLL4 expression, and it may facilitate astrocyte-to-neuronal transformation. (bvsalud.org)
Shown that neurons1
  • In rats it has been shown that neurons often die a full 24 hours after blood flow returns. (wikipedia.org)
Astrocytes3
Oxygen8
  • 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)
  • Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). (wikipedia.org)
  • The main reason for the acute phase of ischemia-reperfusion injury is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. (wikipedia.org)
  • Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced. (wikipedia.org)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
  • S100b counteracts neurodegeneration of rat cholinergic neurons in brain slices after oxygen-glucose deprivation. (uibk.ac.at)
  • Molecular oxygen: friend and foe: the role of the oxygen free radical system in the calcium paradox, the oxygen paradox and ischemia/reperfusion injury. (jamanetwork.com)
  • Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. (cdc.gov)
Inflammation4
Hypoxia-ischemia2
  • We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. (cdc.gov)
  • Global brain hypoxia-ischemia during cardiac arrest has a long-term impact on processing and transfer of sensory information by thalamic circuitry. (cdc.gov)
Microglia1
Tissue6
  • Mitochondrial complex I is thought to be the most vulnerable enzyme to tissue ischemia/reperfusion but the mechanism of damage is different in different tissues. (wikipedia.org)
  • Results After 60 min of tMCAO induction in WT mice, we collected tissue samples at 6, 12, and 24 h after reperfusion. (uni-wuerzburg.de)
  • Reperfusion injury refers to the tissue damage inflicted when blood flow is restored after an ischemic period of more than about ten minutes. (benbest.com)
  • Background and Purpose- Although perfusion abnormality is an increasingly important therapeutic target, the natural history of tissue at risk without reperfusion treatment is understudied. (omicsdi.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)
  • The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)
Reoxygenation1
  • The resuscitation after an HS causes a reperfusion or reoxygenation insult [ 2 - 4 ], gut injury, and multiple organ dysfunctions [ 5 , 6 ]. (medsci.org)
Penumbra6
  • yet at the same time it can induce ischemia-reperfusion injury, which leads to brain damage both in the ischemic core and penumbra area. (spandidos-publications.com)
  • For all patients with complete reperfusion, microstructural integrity changes with lowered MD index were found within the salvaged penumbra for cases of non-BGC usage (mean - 0.02) compared to cases with BGC usage (0.01, p = 0.04). (omicsdi.org)
  • As part of the PENUMBRA SYSTEM, the Penumbra Sterile Aspiration Tubing is indicated to connect the Penumbra Reperfusion Catheters to the Penumbra Aspiration Pump. (penumbrainc.com)
  • Do not use automated high-pressure contrast injection equipment with the Penumbra Reperfusion Catheter because it may damage the device. (penumbrainc.com)
  • Confirm vessel diameter, and select an appropriate size Penumbra Reperfusion Catheter. (penumbrainc.com)
  • Do not use in arteries with diameters smaller or equal to the distal outer diameter of the Penumbra Reperfusion Catheters. (penumbrainc.com)
Extracellular pH2
  • It is assumed that this ionic interplay between TASK and HCN2 channels enhances the resistance of neurons to insults accompanied by extracellular pH shifts. (uni-wuerzburg.de)
  • Within two minutes of ischemia, extracellular pH can drop from about 7.3 to about 6.7. (benbest.com)
Oxidative1
Injury Induced1
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
Vivo1
  • Differential effects of short- and long-term hyperhomocysteinaemia on cholinergic neurons, spatial memory and microbleedings in vivo in rats. (uibk.ac.at)
Infarct volume1
  • RESULTS: Surprisingly, G-1 worsened functional outcomes and increased infarct volume in males poststroke, in association with an increased expression of cleaved caspase-3 in peri-infarct neurons. (monash.edu)
Induces1
Thalamic1
  • Susceptible neuronal populations also include inhibitory neurons in the thalamic Reticular Nucleus. (cdc.gov)
Pyramidal1
  • Danielisova V, Gottlieb M, Nemethova M et al (2009) Bradykinin postconditioning protects pyramidal CA1 neurons against delayed neuronal death in rat hippocampus. (springer.com)
Thalamocortical4
  • For thalamocortical relay neurons, it could be demonstrated that two ion channels, which are predominantly active at rest, strongly influence the resting membrane potential. (biomedcentral.com)
  • We used single neuron recordings and controlled whisker deflections to examine responses of thalamocortical neurons to sensory stimulation in rat survivors of 9 min of asphyxial cardiac arrest incurred on post-natal day 17. (cdc.gov)
  • We found that 48-72 hours after cardiac arrest, thalamocortical neurons demonstrate significantly elevated firing rates both during spontaneous activity and in response to whisker deflections. (cdc.gov)
  • Despite the overall increase in firing, by 6 weeks, thalamocortical neurons display degraded receptive fields, with decreased responses to adjacent whiskers. (cdc.gov)
Neurologic2
  • Postischemic outcome was assessed by determination of overall survival and according to neurologic deficit scores 24 h, 3 days, and 7 days after resuscitation. (asahq.org)
  • However, no differences were observed either in the number of terminal deoxynucleotidyltransferase-mediated d-uracil triphosphate-biotin nick end-labeling-positive cells or viable neurons in the cornu ammonis 1 sector or in the neurologic deficit score when comparing surviving transgenic and nontransgenic rats. (asahq.org)
Brain slices1
  • Effects of cholesterol and its 24S-OH- and 25-OH-oxysterols on choline acetyltransferase-positive neurons in brain slices. (uibk.ac.at)
Vitro1
  • Monocytes deliver bioactive nerve growth factor through a brain capillary endothelial cell-monolayer in vitro and counteract degeneration of cholinergic neurons. (uibk.ac.at)
Acute1
  • Gong L, He J, Sun X, Li L, Zhang X, Gan H. Activation of sirtuin1 protects against ischemia/reperfusion-induced acute kidney injury. (ac.ir)
Methods1
  • METHODS: Initially, we introduced a glial cell marker gene, GFaABC1D, as the promoter within an adeno-associated virus vector overexpressing miR-124 into the motor cortex of an ischemia-reperfusion model in rats. (bvsalud.org)
Neural1
  • My research focuses on the physiological and computational basis of sensory perception and associative learning at the level of individual neurons and their synaptic interactions within complex neural circuits. (ulethbridge.ca)
Glial2
  • Although the majority of works on FMRP have been performed in neurons, it is also found in the developing or mature glial cells including oligodendrocytes, where its function is not well understood. (koreascience.kr)
  • Peripherally administered EPO crosses the blood-brain barrier and activates in the brain anti-apoptotic, anti-oxidant and anti-inflammatory signaling in neurons, glial and cerebrovascular endothelial cells and stimulates angiogenesis and neurogenesis. (biomedcentral.com)
Catheter2
Protects1
Inflammatory5
  • Early reperfusion strategies remain the treatment of choice but can initiate and augment an inflammatory response causing secondary brain damage. (scienceopen.com)
  • The inflammatory response is partially responsible for the damage of reperfusion injury. (wikipedia.org)
  • Some theorize that this delayed reaction derives from the various inflammatory immune responses that occur during reperfusion. (wikipedia.org)
  • Hypothermia has been shown to help moderate intracranial pressure and therefore to minimize the harmful effect of a patient's inflammatory immune responses during reperfusion. (wikipedia.org)
  • Reperfusion injury after myocardial infarction: the role of free radicals and the inflammatory response. (jamanetwork.com)
Immature1
Impairment2
  • Cerebrovascular diseases (CVDs) have become a global public health problem and ischemia‑reperfusion injury, the major cause of neurological impairment exacerbation, is closely related to excitotoxicity. (spandidos-publications.com)
  • Overexpression of miR-124 effectively ameliorated neurological deficits and motor functional impairment in the model rats. (bvsalud.org)
Experimental1
Inhibitor1
  • To this end, the authors generated a transgenic rat line expressing baculovirus p35, a broad-spectrum caspase inhibitor, in central neurons. (asahq.org)
Damage4
  • The severity of these disabilities depends on the ischemia duration, damage expansion, and the affected brain region. (hindawi.com)
  • It was shown that achieving complete reperfusion in a setting of BGC usage with proximal flow arrest minimizes penumbral damage and improves long-term outcomes. (omicsdi.org)
  • A critical coenzyme known as PQQ activates vital cell-signaling pathways involved in creating new mitochondria, improving cellular metabolism, protecting neurons, and repairing DNA damage. (lifeextension.com)
  • Haritaki protected neurons in the experiment when given repeatedly, and in another experiment Haritaki protected against ischemic damage and was shown to be effective in amnesia. (haritaki.club)
NLRP31
  • 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)
Cell death3
Primary1