• These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.com)
  • Neuronal PKD1 inactivation by pharmacological inhibition or lentiviral silencing in vitro, or by genetic inactivation in neurons in vivo, strongly enhances excitotoxic neuronal death. (nature.com)
  • Excitotoxic production of ROS elevates death-associated protein kinase (DAPK) activity, which provokes neuronal apoptosis in cerebral ischemia and seizure models 8 . (nature.com)
  • After hypoxia and ischemia, the production of reactive oxygen species (ROS) rapidly accumulates and leads to mitochondrial dysfunction and delayed neuronal death. (frontiersin.org)
  • Additionally, evidence has revealed that enhancing Sirt1 activity can reduce ROS production, reduce inflammation of neurons and glial cells, so as to reduce neuronal cell death ( 8 ). (frontiersin.org)
  • 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)
  • Regardless of the cause, neuronal ischemia rapidly depletes intracellular adenosine triphosphate (ATP), which leads to failure of the membrane-bound, ATP-dependent ionic channels responsible for neuronal resting membrane potentials and the generation of action potentials. (medscape.com)
  • 0.001) increase in neuronal cell death as well as in the release of tumor necrosis factor alpha, interleukin-1, macrophage inflammatory protein alpha, and RANTES from cultured neurons. (biomedcentral.com)
  • Susceptible neuronal populations also include inhibitory neurons in the thalamic Reticular Nucleus. (cdc.gov)
  • Here, we investigated the role of Sirt1 in the pathogenesis of brain injuries after modulating its activity in primary cultured hippocampal neurons. (frontiersin.org)
  • Recombinant human VEGF-A(165)b exerted neuroprotective effects in response to multiple insults, including glutamatergic excitotoxicity in hippocampal neurons, chemotherapy-induced cytotoxicity of dorsal root ganglion neurons, and retinal ganglion cells (RGCs) in rat retinal ischemia-reperfusion injury in vivo. (bris.ac.uk)
  • Upregulation of HIF-1 expression may play a neuroprotective role in animal models of focal cerebral ischemia ( 6 ). (spandidos-publications.com)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
  • In summary, these results confirmed that Sirt1 is a potent protective factor for neurons subjected to oxidative stress, and the protective effect of Sirt1 is attributed to its regulation of PGC-1α. (frontiersin.org)
  • Previous studies showed that Sirt1 can regulate diabetes-induced cardiac dysfunction and brain ischemic reperfusion injuries by preventing mitochondrial dysfunction and alleviating hepatic steatosis ( 2 - 4 ). (frontiersin.org)
  • Cryonics patients frequently experience ischemic & reperfusion injury between the time when the heart stops and cryostorage begins. (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)
  • I focus my attention on ischemic/reperfusion injury to the brain. (benbest.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)
  • 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)
  • 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)
  • We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. (cdc.gov)
  • 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)
  • Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. (cdc.gov)
  • Previous studies of global brain hypoxia ischemia have primarily focused on injury to the cerebral cortex and to the hippocampus. (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)
  • Reperfusion can also be accompanied by hemorrhagic transformation of the infarct, which is usually related to the volume and site of the infarct, being more common in large cortical infarcts. (medscape.com)
  • Cerebral cortical cultured neurons are pretreated with acetaminophen and then exposed to the superoxide-generating compound menadione (5 μM). (biomedcentral.com)
  • Endogenous expression of human and rat VEGF-A(165)b was detected in hippocampal and cortical neurons. (bris.ac.uk)
  • Extracellular excitatory amino acids are mainly transported into cells by excitatory amino acid transporters (EAATs) expressed on astrocytes to avoid excessive excitation of neurons. (spandidos-publications.com)
  • Within two minutes of ischemia, extracellular pH can drop from about 7.3 to about 6.7. (benbest.com)
  • Approximately 3-4 hours after the onset of ischemia, the integrity of the blood-brain barrier becomes compromised, and plasma proteins are able to pass into the extracellular space. (medscape.com)
  • 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)
  • Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
  • protects both peripheral and central neurons in vivo and in vitro through VEGFR2, MEK1/2, and inhibition of caspase-3 induction. (bris.ac.uk)
  • An initially normal sensory thalamus was repatterned to match the aberrant S1 map by apoptotic deletion of thalamic neurons representing body parts with axons excluded from S1. (nature.com)
  • These data show that acetaminophen has anti-oxidant and anti-inflammatory effects on neurons and suggest a heretofore unappreciated therapeutic potential for this drug in neurodegenerative diseases such as AD that are characterized by oxidant and inflammatory stress. (biomedcentral.com)
  • The proangiogenic VEGF-A(165)a isoform is neuroprotective in hippocampal, dorsal root ganglia, and retinal neurons, but its propermeabitity, vaso-dilatatory, and angiogenic properties limit its therapeutic usefulness. (bris.ac.uk)
  • 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)
  • Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (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)
  • Hypoxic ischemia (HI) involves multiple mechanisms, but the detailed pathogenesis is still unclear. (frontiersin.org)
  • 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)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
  • 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)
  • 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)
  • An ischemic stroke consists of two related pathological injury processes: Primary ischemia-induced brain injury and secondary ischemia reperfusion injury ( 3 ). (spandidos-publications.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)
  • 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)
  • 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 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)
  • Therefore, derivatives of puerarin may serve as promising approach to improve neuron function in ischemia-reperfusion brain injury-related disorders. (hindawi.com)
  • Studies have shown that VaD is frequently caused by ischemia-reperfusion injury. (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)
  • Additionally, neuroprotectants could mitigate the ischemia/reperfusion injury, including edaravone and fingolimod, 3 but their clinical effects cannot achieve the desired condition, primarily due to the rigid blood-brain barrier (BBB) that limits drug delivery to the ischemic regions. (cbinsights.com)
  • 4 On the other hand, a large number of neurons cause irreversible degeneration and necrosis in ischemic regions, which results from ischemia/reperfusion injury. (cbinsights.com)
  • 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)
  • 2009 ) and regulate the Reperfusion Injury Salvage Kinase (RISK) signaling pathway (ERKε, PKC, GSK-3β, STAT3) via cannabinoid receptor 1 (CB1R)(Wang et al. (biomedcentral.com)
  • The ability of the K-opioid receptor agonists U50488H and U62066E (spiradoline mesylate) compared with the non-K close structural analogue U54494A to affect postischemic necrosis of the selectively vulnerable hippocampal CA, neurons was examined in male Mongolian gerbils. (uky.edu)
  • 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)
  • The endogenous nature of VEGF-A(165)b expression suggests that non-isoform-specific inhibition of VEGF-A (for antiangiogenic reasons) may be damaging to retinal and sensory neurons. (bris.ac.uk)
  • The neural crest is present during embryogenesis and gives rise to diverse cell types including enteric neurons and glia, as well as peripheral neurons [ 3 ]. (jcancer.org)
  • 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)
  • However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.com)
  • In contrast, a neuroprotective effect of endogenous VEGF-A(165)b on neurons would be advantageous for neurodegenerative pathologies. (bris.ac.uk)
  • Long-range monosynaptic inputs targeting apical and basal dendrites of primary motor cortex deep output neurons. (edu.hk)
  • In the first minute after stoppage of blood flow to the brain, ATP in neurons is primarily regenerated from ADP by phosphate from PhosphoCreatine ( PCr ). (benbest.com)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
  • High levels of intracellular calcium ion activate proteolytic enzymes (known as calpains) that break down many cell proteins, particularly those in the cytoskeleton of neurons (spectrin, neurofilament and microtubule-associated protein). (benbest.com)
  • In contrast, the role of neurons as a source of inflammatory proteins in the brain has not been examined. (biomedcentral.com)
  • The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)
  • In addition, we document, for the first time, that acetaminophen increases expression of the anti-apoptotic protein Bcl2 in brain neurons and decreases the menadione-induced elevation of the proapoptotic protein, cleaved caspase 3. (biomedcentral.com)
  • Despite the overall increase in firing, by 6 weeks, thalamocortical neurons display degraded receptive fields, with decreased responses to adjacent whiskers. (cdc.gov)