• Hypoxia and ischemia are linked to oxidative stress, which can activate the oxidant-sensitive transient receptor potential ankyrin 1 (TRPA1) channel in cerebral artery endothelial cells, leading to vasodilation. (elifesciences.org)
  • Targeting efficiency was investigated through radiometry, gamma scintigraphy and efficacy was studied in transient middle cerebral artery occlusion (MCAo) rat model. (vitamindwiki.com)
  • Adult male Sprague Dawley rats (n=24) underwent transient middle cerebral artery occlusion (MCAo) 2 weeks before random assignment to either no stereotaxic injection or a stereotaxic injection of either self-assembling silk fibroin hydrogels (4% w/v) or PBS into the lesion cavity. (strath.ac.uk)
  • Sixty rats were subjected to a transient middle cerebral artery occlusion (MCAO). (linc-stg.eu)
  • Because initial neuroprotection is sometimes transient and may not subserve functional recovery, especially on demanding tasks, the authors examined whether postischemic cooling would persistently reduce infarction and forelimb reaching deficits after MCAO. (ox.ac.uk)
  • Endovascular transient middle cerebral artery occlusion (MCAO) with an angiographic microcatheter induced cerebral infarction. (en-journal.org)
  • 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)
  • Wistar rats received right transient middle cerebral artery occlusion (MCAO). (biomedcentral.com)
  • Methods: Transient ischemia was induced by 90 mins middle-cerebral artery occlusion (MCAO) in Sprague-Dawley rats, and LITA or control liposomes given intraperitoneally at occlusion and daily for up to two weeks post-MCAO. (westminster.ac.uk)
  • Na bevestiging van een gebrek aan reactie op staart snuifje in een mannelijke 300 tot 350-gram Sprague Dawley rat, plaats het dier op een 37 graden Celsius verwarmingsplaat en gebruik een rectale sonde voor het toezicht op de kern lichaamstemperatuur. (jove.com)
  • Healthy adult Sprague‑Dawley (SD) male rats were used to establish a control group, sham‑operated group, middle cerebral artery occlusion (MCAO) group, empty virus group and lentivirus group. (spandidos-publications.com)
  • Six-week-old male Sprague-Dawley rats were divided into control (CON), MS model, CIHH treatment (CIHH), and MS + CIHH groups. (cjphysiology.org)
  • In adult male Sprague-Dawley rats, the focal cerebral ischemic injury was induced by middle cerebral artery occlusion (MCAO) models for 1.5 h. (biomedcentral.com)
  • The Sprague-Dawley (SD) rats that underwent right-sided middle cerebral artery occlusion (MCAO) were used for assessment of NKCC1, TNF-α and IL-1β expression using Western blotting, double immunofluorescence and real time RT-PCR, and the model also was used for evaluation of brain water content (BWC) and infarct size. (biomedcentral.com)
  • Thrombosis also form in cerebral venous, which is termed as cerebral venous thrombosis(CVT), a particular type of cerebrovascular disease, characterized by intracerebral hemorrhage and infarction, associated with increased intracranial pressure due to cerebrospinal fluid absorption and cerebral venous drainage, accounting for 0.5-1% of strokes ( 4 ). (frontiersin.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 neurological outcomes, infarction volumes and the level of astroglial and microglial/macrophage hyperplasia, inflammatory cytokine and P2X7R and P2Y1R expression in the peri-infarct hippocampal CA1and sensorimotor cortex were investigated after IS to evaluate the MCAO/R model and therapeutic mechanism of EA treatment. (biomedcentral.com)
  • 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)
  • Postischemic hypothermia also reduces infarction after middle cerebral artery occlusion (MCAO) in rat. (ox.ac.uk)
  • 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)
  • 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)
  • Cerebral ischemia-reperfusion (IR) triggers lipid peroxidation and inflammation, which exacerbate injury. (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)
  • Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. (sciencegate.app)
  • Cerebral ischemia/reperfusion (I/R) injury is closely related to dysfunctional glucose metabolism. (sciencegate.app)
  • This study aimed to evaluate the possible protective effect of platelet-rich plasma (PRP) on ischemia reperfusion (I/R)-induced ovarian injury in a rat model. (cjphysiology.org)
  • Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (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)
  • 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)
  • Most result from middle cerebral artery occlusion (MCAO) causing damage to striatum and cortex resulting in long-term disability. (cdc.gov)
  • To this end we analyzed the proteomic profile of cortex and striatum at 2 and 12 h following occlusion via isobaric tag for relative and absolute quantification (iTRAQ) with liquid chromatography-tandem mass spectrometry (LCMS/ MS). Our proteomic analysis identified several key proteins altered by ischemia in a time-related fashion as well as by repeated sleep restriction exposure. (cdc.gov)
  • These RAS peptides are present in astrocytes, glial cells, oligodendrocytes, and neurons of various areas of the brain [ 14 , 15 ] such as the basal ganglia, cerebral cortex, and hippocampus [ 16 ]. (hindawi.com)
  • The lesion was localized in the middle cerebral artery territory, including the sensorimotor cortex. (en-journal.org)
  • Adequacy of MCAO and reperfusion was monitored with laser-Doppler flowmetry over the ipsilateral parietal cortex. (utmb.edu)
  • Infarct volume in the cortex and caudoputamen (CP) complex was assessed by triphenyl tetrazolium chloride staining at 72 hours after MCAO. (utmb.edu)
  • This study aimed to explore if alleviation of cerebral edema by 10% HS might be effected through down-regulation of inflammatory mediator expression in the microglia, and thus result in decreased NKCC1 expression in astrocytes in the cerebral cortex bordering the ischemic core. (biomedcentral.com)
  • Later, rats underwent 90 minutes of normothermic MCAO, through a microclip, or sham operation. (ox.ac.uk)
  • Five groups of animals were designed: sham (underwent surgery without MCAO) and MCAO groups, the MCAO groups were pretreated orally by gavages with RHE (50, 75, and 100 mg/Kg/day), daily for 30 days. (nih.gov)
  • 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)
  • Hypoxia caused dilation of cerebral arteries, which was disrupted by antioxidants, TRPA1 blockade and by endothelial cell-specific Trpa1 deletion ( Trpa1 ecKO mice). (elifesciences.org)
  • Loss of TRPA1 channels in endothelial cells increased cerebral infarcts, whereas TRPA1 activation with cinnamaldehyde reduced infarct in wildtype, but not Trpa1 ecKO, mice. (elifesciences.org)
  • Pires and Earley studied TRPA1 channels in brain arteries from mice. (elifesciences.org)
  • With these webinar opportunities, Cyagen's expert team will comprehensively explain the cutting-edge technology, academic hotspots, and application limitations of animal models - such as genetically modified, humanized, and immunodeficient mice - from various perspectives, as we aim to exchange and share valuable experiences with you and your team. (cyagen.com)
  • The MCAO mice were exposed to Sevo or injected with miR-203-3p- or HDAC4-related plasmids. (engreen.com.cn)
  • MCAO mice presented down-regulated miR-203-3p and up-regulated HDAC4. (engreen.com.cn)
  • Sevo improved neurological function, brain pathological damage and reduced neuronal apoptosis and inflammation in MCAO mice, while overexpressing miR-203-3p further enhanced those effects. (engreen.com.cn)
  • HDAC4 overexpression antagonized the impacts of miR-203-3p up-regulation on MCAO mice. (engreen.com.cn)
  • It is clearly elucidated that miR-203-3p enhances the protective effects of Sevo on MCAO mice through elevating Bcl-2 and down-regulating HDAC4, potentially and clinically offering an effective treatment method with Sevo for cerebral ischaemic injury. (engreen.com.cn)
  • Importantly, PAC KO mice exhibited significantly smaller brain infarct volume when subjected to a middle cerebral artery occlusion (MCAO) stroke model. (hopkinsyidp.org)
  • Accumulated evidence suggests that thalidomide suppresses nerve cell death in neurologic model mice. (elsevierpure.com)
  • Oxidative stress is an important activator of PKD1 in cellular models, but its capacity to activate this kinase in vivo is largely unknown. (nature.com)
  • This in vivo stroke model confirmed that self-assembling silk fibroin hydrogels provide a favourable microenvironment as a future support matrix in the stroke cavity. (strath.ac.uk)
  • Ischemia models used include but are not limited to , middle cerebral artery occlusion (MCAO) and hypoxic-ischemic encephalopathy (HIE) animal models in vivo , and oxygen-glucose deprivation (OGD) in vitro for neuronal/microglial culture. (uth.edu)
  • Brain glutamate levels were determined by in vivo MR spectroscopy (MRS) during artery occlusion (80 min) and reperfusion (180 min). (linc-stg.eu)
  • In vivo diffusion tensor imaging (DTI) of the stroke lesion to assess the neuroplastic changes and fiber tractography demonstrated three-dimensional patterns in the corticospinal tract 12 weeks after MCAO. (en-journal.org)
  • Delayed but prolonged hypothermia persistently decreases cell death and functional deficits after global cerebral ischemia in rodents. (ox.ac.uk)
  • We used a cerebral ischemia rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). Thalidomide treatment significantly decreased the infarct volume and neurological deficits of MCAO/R rats. (elsevierpure.com)
  • Methods - Halothane-anesthetized adult male and female Wistar rats (250 to 275 g) were subjected to 2 hours of middle cerebral artery occlusion (MCAO) by the intraluminal suture technique. (utmb.edu)
  • Ligate the suture of the external carotid artery that is thin and loose knot and cut off the external carotid artery. (jove.com)
  • Loosen the loose knot of the internal carotid artery and continue inserting the thread bolt to the beginning of the middle cerebral artery marked with the suture and cut off the exposed thread bolt. (jove.com)
  • A middle cerebral artery occlusion (MCAO) mouse model was established by nylon suture method. (engreen.com.cn)
  • To test the neuroprotective efficacy of 5-LOX inhibition in a rat model of focal cerebral IR, ischemic animals were either pre- or post-treated with a potent selective 5-LOX inhibitor, (N- [3-[3-(-fluorophenoxy) phenyl]-1-methyl-2-propenyl]- N -hydroxyurea (BW-B 70C). (biomedcentral.com)
  • In the present study, we used a 5-LOX inhibitor, N- [3-[3-(-fluorophenoxy) phenyl]-1-methyl-2-propenyl]- N -hydroxyurea (BW-B 70C), in a rat model of focal cerebral IR. (biomedcentral.com)
  • Neuronally derived NO has been shown to be deleterious in the male but not in the female rodent model of focal ischemic stroke. (utmb.edu)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
  • IS refers to the stenosis or occlusion of cerebral blood vessels, leading to the blockage of cerebral blood flow, which in turn causes ischemia, hypoxia, softening, and even necrosis of brain tissue, thereby resulting in cerebrovascular dysfunction and irreversible brain damage [ 6 , 7 ]. (hindawi.com)
  • We hypothesized that TRPA1 channels in endothelial cells are activated by hypoxia-derived reactive oxygen species, leading to cerebral artery dilation and reduced ischemic damage. (elifesciences.org)
  • Using isolated cerebral arteries expressing a Ca 2+ biosensor in endothelial cells, we show that 4-hydroxynonenal and hypoxia increased TRPA1 activity, detected as TRPA1 sparklets. (elifesciences.org)
  • 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)
  • Our previous study demonstrated that chronic intermittent hypobaric hypoxia (CIHH) protects vascular endothelium function through ameliorating autophagy in mesenteric arteries of metabolic syndrome (MS) rats. (cjphysiology.org)
  • Excitotoxic production of ROS elevates death-associated protein kinase (DAPK) activity, which provokes neuronal apoptosis in cerebral ischemia and seizure models 8 . (nature.com)
  • SUF also inhibited caspase3 and Bax rats and promoted Bcl2 in MCAO rats, thus inhibiting cell apoptosis. (sciencegate.app)
  • Conclusions - These data: (1) demonstrate that this dose of selective KOR agonist provides ischemic neuroprotection in male but not female rats, (2) demonstrate that the lack of protection by BRL is not attributable to circulating ovarian hormones, and (3) highlight the importance of using animal models of both sexes in preclinical studies of experimental ischemia. (utmb.edu)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
  • The results suggest that 10% HS alleviates cerebral edema through inhibition of the NKCC1 Cotransporter, which is mediated by attenuation of TNF-α and IL-1β stimulation on NKCC1. (biomedcentral.com)
  • 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)
  • Rats were euthanized at day 15 after MCAO for mRNA level evaluation of ischemic infarct area, endogenous neurogenesis, angiogenesis, and expression of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF). (biomedcentral.com)
  • This study suggests that combination therapy of intracerebral transplantation SB623 cells and voluntary exercise with RW achieves robust neurological recovery and synergistically promotes endogenous neurogenesis and angiogenesis after cerebral ischemia, possibly through a mechanism involving the up-regulation of BDNF and VEGF. (biomedcentral.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)
  • Our previous research confirmed that electroacupuncture (EA) stimulus elicits neuroprotective effects against cerebral ischemic injury through α7 nicotinic acetylcholine receptor (α7nAChR)-mediated inhibition of high-mobility group box 1 release mechanism. (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)
  • The purpose of this study is to investigate the effect of sufentanil (SUF) on CIRI model rats. (sciencegate.app)
  • 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)
  • The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. (ewha.ac.kr)
  • Maximum infarct volume was exhibited over the first week after MCAO, which progressively inhibited ischemic core expansion, manifested by enhanced functional recovery of the affected hand over 12 weeks after MCAO. (en-journal.org)
  • Our findings demonstrate the recovery of fine motor skill after stroke, and outline the behavioral characteristics and features of functional disorder of NHP stroke model, providing a basis for assessing hand motor function after stroke. (en-journal.org)
  • Behavioral tests were performed at day 1, 7, and 14 after MCAO using the modified Neurological Severity Score (mNSS) and cylinder test. (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)
  • In a passive ITP mouse model, macrophage-specific depletion of Mst4 reduced the numbers of M1 macrophages in the spleen and peritoneal lavage fluid, attenuated the expression of M1 cytokines, and promoted the predominance of FcγRIIb in splenic macrophages, which resulted in amelioration of thrombocytopenia. (bvsalud.org)
  • SUF pretreatment also effectively reduced the expression of inflammatory cytokines in MCAO rats, including interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10 and tumor necrosis factor (TNF)-α. (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)
  • Hypertonic saline (HS) has been successfully used clinically for treatment of various forms of cerebral edema. (biomedcentral.com)
  • Up-regulated expression of Na-K-Cl Cotransporter 1 (NKCC1) and inflammatory mediators such as tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) has been demonstrated to be closely associated with the pathogenesis of cerebral edema resulting from a variety of brain injuries. (biomedcentral.com)
  • At 1 hour after MCAO, volumetric mismatch detected smaller volumes of penumbra in both strains (SHRSP: 31 +/- 50 mm(3), WKY: 22 +/- 59 mm(3), mean +/- s.d.) compared with spatial assessment (SHRSP: 36 +/- 15 mm(3), WKY: 43 +/- 43 mm(3)) and ADC lesion expansion (SHRSP: 41 +/- 45 mm(3), WKY: 65 +/- 41 mm(3)), although these differences were not statistically significant. (sinapse.ac.uk)
  • Infarct volumes were assessed by magnetic resonance imaging (MRI) before treatment administration, and 24 h and 7 days after MCAO. (linc-stg.eu)
  • According to the World Health Organization, cerebral ischaemia is the second leading cause of death and the third leading cause of disability in the world [ 1 ]. (biomedcentral.com)
  • 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)
  • Stroke is caused not only by arterial thrombosis but also by cerebral venous thrombosis. (frontiersin.org)
  • The molecular pathological hallmarks of arterial stroke and cerebral venous thrombosis. (frontiersin.org)
  • Ischemic stroke results from arterial occlusion and can cause irreversible brain injury. (en-journal.org)
  • In this study, we aimed to clarify whether combination therapy of intracerebral transplantation of human modified bone marrow-derived MSCs, SB623 cells, and voluntary exercise with running wheel (RW) could exert synergistic therapeutic effects on a rat model of ischemic stroke. (biomedcentral.com)
  • This suggests that ion channel transporters related to water transport whose expression is localized in astrocytes and other cerebral cell types are potential therapeutic targets in HS treatment. (biomedcentral.com)
  • Expression of SOX9 did not decrease during aging and was instead upregulated by reactive astrocytes in a number of settings, including a murine model of amyotrophic lateral sclerosis (SOD1G93A), middle cerebral artery occlusion, and multiple mini-strokes. (jneurosci.org)
  • During the early stage of cerebral I/R injury, significantly-swollen mitochondria decrease adenosine triphosphate (ATP) and produce excessive reactive oxygen species (ROS) and oxidative stress, finally resulting in cell death [ 6 ]. (biomedcentral.com)
  • Furthermore, phosphosynapsin may play some role in the synaptic plastic adaptations before or during reactive synaptogenesis after the MCAO. (ewha.ac.kr)
  • The study demonstrates the neuroprotective potential of 5-LOX inhibition through down-regulation of NF-κB in a rat model of experimental stroke. (biomedcentral.com)
  • 2013 ). In addition, we demonstrated that EA could attenuate cerebral ischemic injury via regulation of α7nAChR-mediated inhibition of HMGB1 release in rats (Wang et al. (biomedcentral.com)
  • Human recombinant glutamate oxaloacetate transaminase 1 (GOT1) supplemented with oxaloacetate induces a protective effect after cerebral ischemia. (linc-stg.eu)
  • However, the protective effect of the administration of the recombinant GOT1 (rGOT1) enzyme has not been yet addressed in cerebral ischemia. (linc-stg.eu)
  • The aim of this study was to analyze the protective effect of an effective dose of oxaloacetate and the human rGOT1 alone and in combination with a non-effective dose of oxaloacetate in an animal model of ischemic stroke. (linc-stg.eu)
  • Magnetic Resonance Imaging (MRI) of the ischemic model confirmed better efficacy of Vitamin D3-Nanoemulsion. (vitamindwiki.com)
  • Magnetic resonance imaging (MRI) was used to estimate lesion volume at 24 h, 1 and 2 weeks post-MCAO and anterior lateral ventricular volume (ALVv) at 2 weeks post-MCAO. (westminster.ac.uk)
  • SB623 cells (4.0 × 10 5 cells/5 μl) were stereotactically injected into the right striatum at day 1 after MCAO. (biomedcentral.com)
  • G-protein-coupled receptors and ion channels present on the endothelial cells and vascular smooth muscle cells (SMCs) that form the walls of cerebral blood vessels initiate many of the signaling cascades that enable these intrinsic adaptive processes. (elifesciences.org)
  • A rat MCAO model was established to evaluate the pharmacodynamics of SHD in the treatment of IS, and Western blot analysis assessed the level of proteins in the related pathways. (hindawi.com)
  • Animal modeling has a played a prominent role in traditional scientific research for hundreds of years, and more recently, inbred strains have been developed to support genetically modified models for applications in biomedical and health research. (cyagen.com)
  • Dr. Steve Yu has more than 20 years of experience in the field of genetically modified animal models from both R&D and management roles. (cyagen.com)
  • As an internationally renowned expert in model animals and cell biology, Dr. Yu successively served in Yale School of Medicine and NYU Grossman School of Medicine, inGenious Targeting Laboratory (iTL), Applied StemCell (ASC) and other institutions in the field of genetically modified animal models. (cyagen.com)
  • Currently, Dr. Yu is working for Cyagen as Senior Vice President and Senior Scientist, primarily responsible for the technical development of genetically modified animal model platforms. (cyagen.com)
  • By using genetically modified animal models, we study escapee genes that escape from X chromosome inactivation (XCI), and try to understand whether and how these genes impacts on the sexual dimorphism. (uth.edu)
  • The mechanism of action of Sanhua Decoction (SHD) in the treatment of ischemic stroke (IS) was analyzed based on the network pharmacology technology, and the pharmacodynamics and key targets were verified using the rat middle cerebral artery occlusion (MCAO) model. (hindawi.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)