Middle cerebral arteryOcclusionGlobal cerebral ischemiaApoptosisNeuronalRetinal neuronsNeuroprotectiveDamage after ceBrain NeuronsRats with cerebralHypoxia ischemiaFocal ischemiaCentral neuronsCortical neuronsHippocampal CA1 regionTherapeuticHippocampusInfarctionCardiac arrestMurineNeurologicalOxidative stressGlial cellsAstrocytesStrokeAcute cerebralNeurodegenerativePenumbraEntericCytokinesThalamicExtracellularVivoNecrosisPrimaryProtectsAdultInhibitionProteinsDeficitsProcessesProtectiveMetabolicTissueDopamineViableDysfunctionMethods
Middle cerebral artery4
- 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)
- Sprague-Dawley rats were used as experimental animals, and middle cerebral artery occlusion was used to make cerebral ischemia/reperfusion model. (molecularhydrogenstudies.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)
- Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice. (scienceopen.com)
Occlusion3
- 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)
- Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. (nih.gov)
- Global cerebral ischemia was performed via 10 min of four-vessel occlusion. (springer.com)
Global cerebral ischemia8
- Global cerebral ischemia followed by reperfusion, which leads to extensive neuronal damage, particularly the neurons in the hippocampal CA1 region. (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)
- 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)
- 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)
Apoptosis8
- A study has shown that neurons in the ischemic penumbra may undergo apoptosis hours or days after ischemia and alleviating ischemia reperfusion injury is an achievable therapeutic goal in the early intervention of ischemic stroke aimed at limiting the amount of infarction ( 4 ). (spandidos-publications.com)
- Apoptosis is one of the major mechanisms that lead to neuronal death after cerebral ischemia and reperfusion. (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)
- Ding ZM, Wu B, Zhang WQ et al (2012) Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the same effect on inhibition of apoptosis. (springer.com)
- Yuan Y, Guo Q, Ye Z et al (2011) Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (springer.com)
- TTC, Nissl, and TUNEL staining showed the significant improvement of infarction volume, neuron morphology, and neuron apoptosis in rat with hydrogen treatment. (molecularhydrogenstudies.com)
- Figure 6: Top-down plasticity repatterns the VPN through exaggerated apoptosis that is selective for VPN neurons representing body parts deleted from S1 in cKO mice. (nature.com)
- Accumulating evidence suggests that electro-acupuncture at the Governor vessel enhances vascular endothelial growth factor expression and inhibits cellular apoptosis following acute cerebral ischemic/reperfusion injuries. (beikecelltherapy.com)
Neuronal6
- These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.com)
- We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. (nih.gov)
- Danielisova V, Gottlieb M, Nemethova M et al (2009) Bradykinin postconditioning protects pyramidal CA1 neurons against delayed neuronal death in rat hippocampus. (springer.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)
- 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)
Retinal neurons1
- 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)
Neuroprotective9
- 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)
- Similarly, midiv-1 has demonstrated neuroprotective effects by greatly reducing neuron death due to seizure. (wikipedia.org)
- The neuroprotective effects of remifentanil preconditioning against cerebral ischemia/reperfusion injury have been recently reported. (springer.com)
- Jeong S, Kim SJ, Jeong C et al (2012) Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats. (springer.com)
- Upregulation of HIF-1 expression may play a neuroprotective role in animal models of focal cerebral ischemia ( 6 ). (spandidos-publications.com)
- 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)
- 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)
- In contrast, a neuroprotective effect of endogenous VEGF-A(165)b on neurons would be advantageous for neurodegenerative pathologies. (bris.ac.uk)
- 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)
Damage after ce1
- Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)
Brain Neurons2
- 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)
- However, a clear connection between exposure to oxidative stress and release of inflammatory mediators in brain neurons has not been shown. (biomedcentral.com)
Rats with cerebral1
- 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)
Hypoxia ischemia5
- Autophagy is a process that relies on lysosomal pathways for the degradation of cytoplasmic proteins and organelles and plays an important role in the pathology of brain injury such as hypoxia ischemia[ 3 ]. (ijpsonline.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)
- 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)
Focal ischemia1
- Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (springer.com)
Central neurons2
- protects both peripheral and central neurons in vivo and in vitro through VEGFR2, MEK1/2, and inhibition of caspase-3 induction. (bris.ac.uk)
- To this end, the authors generated a transgenic rat line expressing baculovirus p35, a broad-spectrum caspase inhibitor, in central neurons. (asahq.org)
Cortical neurons3
- Endogenous expression of human and rat VEGF-A(165)b was detected in hippocampal and cortical neurons. (bris.ac.uk)
- 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)
Hippocampal CA1 region1
- 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)
Therapeutic1
- 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)
Hippocampus2
- Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. (nih.gov)
- Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6-12 hours) after ischemia. (nih.gov)
Infarction1
- 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)
Cardiac arrest6
- Midiv-1 has been demonstrated to attenuate the effects of ischemia reperfusion injury after cardiac arrest. (wikipedia.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)
- 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)
- If treated with cardiopulmonary resuscitation, however, cardiac arrest is survivable, but survivors often show evidence of injury in selectively vulnerable regions of the brain. (cdc.gov)
Murine1
- 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)
Neurological3
- 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)
- Inhibition of HSP90β expression improved neurological deficits and alleviated brain injury by increasing EAAT2 expression. (spandidos-publications.com)
- In one study, patients who took 1,200 mg/day of NAC in combination with weekly intravenous NAC, had better neurological health and improvement in midbrain dopamine neurons. (traceminerals.com)
Oxidative stress3
- 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)
- Neurotoxic factors such as amyloid beta (Aβ) evoke oxidative stress and directly injure neurons [ 14 ]. (biomedcentral.com)
- Previously, we demonstrated that the protein kinase Hippo/MST1 plays an important role in oxidative stress-induced cell death in mammalian primary neurons and that the protein kinase c-Abl phosphorylates MST1 at Y433, which increases MST1 kinase activity. (ox.ac.uk)
Glial cells2
- Outer radial glial cells (oRGs) give rise to neurons and glial cells and contribute to cell migration and expansion in developing neocortex. (nanostring.com)
- In bilirubin toxicity, the primary targets are glial cells and neurons. (bakirkoymedj.org)
Astrocytes5
- 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)
- Bi-directionally protective communication between neurons and astrocytes under ischemia. (edu.hk)
- The cytotoxic effect of bilirubin has been demonstrated in various cell types, including astrocytes and neurons. (bakirkoymedj.org)
- Among nerve cells, neurons were shown to be more susceptible to the toxic effects of bilirubin than astrocytes (3,4). (bakirkoymedj.org)
- Astrocytes, the most intense cell group in the brain, are critically important in protection of the central nervous system as they provide metabolic and trophic support to neurons, which also contribute to form blood-brain barrier. (bakirkoymedj.org)
Stroke4
- 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 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)
- IVIg treatment protected neurons in experimental stroke models by a mechanism involving suppression of NLRP1 and NLRP3 inflammasome activity. (scienceopen.com)
- Specific deletion of MST1 in microglia mitigates stroke-induced brain injury. (ox.ac.uk)
Acute cerebral1
- Hippo/MST1 signaling mediates microglial activation following acute cerebral ischemia-reperfusion injury. (ox.ac.uk)
Neurodegenerative1
- In newborns the insufficient antioxidant defense mechanisms contribute to the development of cerebral ischemia, excitotoxicity and neurodegenerative processes in the nervous system (3). (bakirkoymedj.org)
Penumbra2
- 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)
- In the early stage of ischemia and hypoxia, cells will increase the energy supply to the ischemic area, especially the functional area of the ischemic penumbra, by regulating glycolysis. (ijpsonline.com)
Enteric2
- 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)
- These results indicated that the jejunal ischemic-reperfusion injury affected the neurons of the enteric nervous system and resulted in early decrease in the activity of the nitric oxide neurotransmitter one hourafterthe injury. (csgh.info)
Cytokines1
Thalamic1
- 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)
Extracellular1
- Within two minutes of ischemia, extracellular pH can drop from about 7.3 to about 6.7. (benbest.com)
Vivo1
- Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
Necrosis1
- 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)
Primary1
Protects3
- Zhou Y, Fathali N, Lekic T et al (2012) Remote limb ischemic postconditioning protects against neonatal hypoxic-ischemic brain injury in rat pups by the opioid receptor/Akt pathway. (springer.com)
- Zhang Y, Irwin MG, Wong TM (2004) Remifentanil preconditioning protects against ischemic injury in the intact rat heart. (springer.com)
- Questionable whether intermittent fasting (IF) protects against ischemic brain injury. (il-13.com)
Adult3
- In this study it shows that electro-acupuncture at Conception and Governor vessels continuously promoted the proliferation and differentiation of adult stem cells into neurons in cerebral ischemia/reperfusion in rats. (beikecelltherapy.com)
- Experimental animals, adult male Wistar rats, were divided into three groups according to the reperfusion period after previous ischemic episode lasting for one hour. (csgh.info)
- Because of the increased ability of the immature myocardium to rely on anaerobic glycolysis, it can withstand ischemic injury better than adult myocardium can. (medscape.com)
Inhibition2
- 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 basic cellular mechanism is the inhibition of oxidative phosphorylation in neurons (1-3). (bakirkoymedj.org)
Proteins2
- 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)
Deficits1
- Morris water maze task was used to quantify spatial learning and memory deficits after reperfusion. (springer.com)
Processes2
- 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)
- In addition, the addition of VEGF to the culture medium can increase the survival rate of neurons in the cerebral cortex as well as the number and length of ganglion cell processes, to promote nerve growth. (spandidos-publications.com)
Protective3
- Puerarin has shown protective effect on injury of neural cell. (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)
- Inflammation is a protective physiological response of an organism to chemical, physical, infectious agents, environmental toxins, ischemia or an antigen-antibody interaction. (biomedcentral.com)
Metabolic1
- Most of the metabolic energy of neurons is expended on maintaining ion gradients across the cell membrane. (benbest.com)
Tissue2
- 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)
- Multi-protein complexes called inflammasomes have recently been identified and shown to contribute to cell death in tissue injury. (scienceopen.com)
Dopamine1
- While I started my career as a developmental neurobiologist and pediatric neurologist interested in how dopamine was affected during early brain injury, I shifted my research focus radically nearly 25 years ago in an attempt to repurpose already FDA-approved medicines for the treatment of neurologic disease associated with HIV-1 infection. (rochester.edu)
Viable1
- 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)
Dysfunction1
- Enhanced Activity of Exportin-1/CRM1 in Neurons Contributes to Autophagy Dysfunction and Senescent Features in Old Mouse Brain. (courtlab.cl)