• 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)
  • 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)
  • Oxidative stress-mediated mitochondrial damage has been shown to be involved in apoptosis. (frontiersin.org)
  • RSV can improve mitochondrial function, reduce oxidative stress in podocytes, and inhibit apoptosis induction through the Sirt1/PGC-1a axis ( 12 ). (frontiersin.org)
  • 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)
  • The studies focusing on the oxidative stress-induced damages verified the cardioprotective theory and showed that both endogenous PACAP production and exogenous PACAP treatment leaded to decreased apoptosis of heart muscle cells. (hungarica.eu)
  • Its pathophysiological mechanisms involve various biological events such as neuronal apoptosis, oxidative stress, endoplasmic reticulum stress and inflammatory cascade[ 2 - 5 ]. (ijpsonline.com)
  • 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 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)
  • Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
  • Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (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)
  • Jeong S, Kim SJ, Jeong C et al (2012) Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats. (springer.com)
  • The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase‑3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane‑induced newborn rats. (spandidos-publications.com)
  • Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane‑induced neuronal apoptosis through HIF‑1α‑, VEGF‑ and p38‑associated signaling pathways in newborn rats. (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)
  • 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)
  • Inhalation of water electrolysis-derived hydrogen ameliorates cerebral ischemia-reperfusion injury in rats: a possible new hydrogen resource for clinical use. (molecularhydrogenstudies.com)
  • 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)
  • Acetaminophen reduces mitochondrial dysfunction during early cerebral postischemic reperfusion in rats. (harvard.edu)
  • 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)
  • However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.com)
  • 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)
  • Global cerebral ischemia followed by reperfusion, which leads to extensive neuronal damage, particularly the neurons in the hippocampal CA1 region. (springer.com)
  • 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)
  • Here, we investigated the role of Sirt1 in the pathogenesis of brain injuries after modulating its activity in primary cultured hippocampal neurons. (frontiersin.org)
  • In this study, we found that HWTX-I potently inhibited sodium channels in rat hippocampal and cockroach dorsal unpaired median (DUM) neurons with the IC(50) values of 66.1±5.2 and 4.80±0.58nM, respectively. (smartox-biotech.com)
  • HWTX-I exhibited no effect on the steady-state activation and inactivation of sodium channels in rat hippocampal and cockroach DUM neurons. (smartox-biotech.com)
  • In this re- search, hippocampal neurons were cultured and treated with mild hypothermia and Ac-DEVD-CHO after oxygen- glucose deprivation (OGD). (syksignal.com)
  • Our previous research showed that mild hypothermia can inhibit the activation of oxygen-glucose deprivation (OGD)-induced caspase-3 injury in a rat hippocampal neuron model [12], while the role of caspase-3 in the protective molecular mechanism of mild hy- pothermia against OGD injury remains uncertain. (syksignal.com)
  • By comparing the protective effects of mild hypothermia and Ac- DEVD-CHO (a caspase-3 inhibitor) against OGD, our current study was designed to determine whether inhibiting the activation of caspase-3 is involved in the main and common molecular mechanism of mild hy- pothermia in protecting hippocampal neurons from OGD injury. (syksignal.com)
  • Hippocampal neurons in primary culture were used for this study. (syksignal.com)
  • These behavioral upturns were associated with increased intact neurons (Nissl stain) and a reduction in OVX/D-Gal-mediated hippocampal CA1 neurodegeneration and astrocyte activation assessed as GFAP immunoreactivity. (fue.edu.eg)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
  • 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)
  • 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)
  • 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)
  • Compared to the oxygen-glucose deprivation/reperfusion group, the protein and mRNA expressions of p-JNK, Bax, cleaved Caspase3 was decreased significantly. (archive.org)
  • Neuroglobin overexpression inhibits oxygen-glucose deprivation-induced mitochondrial permeability transition pore opening in primary cultured mouse cortical neurons. (harvard.edu)
  • 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)
  • The neuroprotective effects of remifentanil preconditioning against cerebral ischemia/reperfusion injury have been recently reported. (springer.com)
  • Upregulation of HIF-1 expression may play a neuroprotective role in animal models of focal cerebral ischemia ( 6 ). (spandidos-publications.com)
  • These findings suggested that MQ exerts a neuroprotective effect in cerebral ischemia by blocking apoptosis via the p-JNK/Bax pathway. (archive.org)
  • Neuronal loss in the hippocampus, regarded as one of the basic pathological mechanisms underlying cognitive impairment, can result from Focal cerebral ischemia-reperfusion. (medindia.net)
  • 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)
  • 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)
  • Inflammation is a protective physiological response of an organism to chemical, physical, infectious agents, environmental toxins, ischemia or an antigen-antibody interaction. (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)
  • Efferocytosis of apoptotic neurons by macrophages is essential for the resolution of inflammation and for neuronal protection from secondary damage. (thno.org)
  • Studies also show that Sirt1 regulates apoptosis through other pathways, such as the anti-inflammatory pathway of NF-κB acetylation and the regulation of AMPK in autophagy ( 6 , 7 ). (frontiersin.org)
  • Therefore, in this review, we avoid a lengthy repetition of the description of autophagy and cell death processes and focus on the death-promoting roles of autophagy and the intertwined connection between autophagy and apoptosis. (nature.com)
  • 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)
  • There is colocalization between phosphorylated eIF2α and cytosolic cytochrome c, which is released from mitochondria in apoptosis. (wikipedia.org)
  • Octyl gallate reduces ATP levels and Ki67 expression leading HepG2 cells to cell cycle arrest and mitochondria-mediated apoptosis. (harvard.edu)
  • Mitochondria are known to be central to the cell's response to ischemia, because of their role in energy generation, in free radical generation, and in the regulation of apoptosis. (starrlifesciences.com)
  • 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)
  • PQQ has previously been shown to promote growth of new mitochondria within aging cells, 1-3 up-regulate cellular metabolism, 1,2 protect neurons, 4-7 and repair DNA! (lifeextension.com)
  • 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)
  • In contrast to findings in males, G-1 reduced neurological deficit, apoptosis, and infarct volume in ovariectomized females, but had no significant effect in intact females. (monash.edu)
  • 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)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
  • Many studies have found that MH improves the neurological function of patients with HIE by reducing neuronal apoptosis [7,8]. (syksignal.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)
  • 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)
  • 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)
  • 2018 ). NLRP3 inflammasome is composed of NLRP3 (nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3), ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain) and procaspase-1, subsequently amplifying the production and secretion of proinflammatory cytokines, apoptotic and pyroptotic cell deaths(Zhong et al. (biomedcentral.com)
  • 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)
  • Apoptosis is the result of a biochemical cascade and caspase pro- teases are major participants in the apoptotic program [9]. (syksignal.com)
  • In addition, apoptosis was examined using cleaved caspase-3 immunohistochemistry. (monash.edu)
  • 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)
  • In conclusion, caspase-3 serves as a key intervention point of the key modulation site or regulatory region in MH treatment that protects neuronal apoptosis against OGD injury. (syksignal.com)
  • Given the role of caspases in apoptosis, caspase inhibitors may provide neuronal protection after cardiac arrest. (asahq.org)
  • Hypoxic ischemia (HI) involves multiple mechanisms, but the detailed pathogenesis is still unclear. (frontiersin.org)
  • 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)
  • 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)
  • 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)
  • An ischemic stroke consists of two related pathological injury processes: Primary ischemia-induced brain injury and secondary ischemia reperfusion injury ( 3 ). (spandidos-publications.com)
  • We evaluated functional and histological end points of stroke outcome up to 72 hours after ischemia-reperfusion. (monash.edu)
  • Graphical presentation of the various stages of cerebral ischemia stroke, i.e., acute phase, subacute phase, and chronic phase and their contributing factors. (hindawi.com)
  • 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)
  • The dysfunction is associated with issues with apoptosis and normal cellular metabolic regulation, all regulated through OPA1. (thermofisher.com)
  • These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.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)
  • Earlier studies have shown that proliferation of endogenous neural precursor cells cannot alone compensate for the damage to neurons and axons. (medindia.net)
  • 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)
  • Complete reperfusion in a setting of balloon guide catheter minimizes penumbral damage and improves long-term outcome. (omicsdi.org)
  • Apoptosis is one of the major mechanisms that lead to neuronal death after cerebral ischemia and reperfusion. (springer.com)
  • The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. (spandidos-publications.com)
  • The present study was undertaken to study the effects of exogenous H2S on ischemia/reperfusion (I/R) injury of spinal cord and the underlying mechanisms. (biomedcentral.com)
  • 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)
  • As a molecular chaperone, HSP90 regulates the conformational maturation and functional stability of many signaling proteins in cells, serves important roles in cell growth, differentiation, apoptosis and tumor development and is an important antitumor target ( 8 , 9 ). (spandidos-publications.com)
  • Countering NADH production, calcium action on the mitochondrial permeability transition pores increases inner membrane permeability thereby reducing proton potential, causing the matrix to swell and ultimately releasing cytochrome c (an initiator of apoptosis). (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)
  • 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)
  • Danielisova V, Gottlieb M, Nemethova M et al (2009) Bradykinin postconditioning protects pyramidal CA1 neurons against delayed neuronal death in rat hippocampus. (springer.com)
  • It was previously believed that the main pathogenic mechanism of PD was the loss of dopaminergic neurons and most researchers considered that the therapeutic effect of MSCs on PD was attributable to their cell replacement ability [ 21 , 22 ]. (biomedcentral.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)
  • Cell viability and apoptosis were evaluated in both prophylaxis and treatment groups after the procedure. (bakirkoymedj.org)
  • There was a 50% decrease in cell viability and a five-fold increase in apoptosis in the bilirubin 10 group compared with the control group (p˂0.001, p˂0.001). (bakirkoymedj.org)
  • EGB-761 given for prophylaxis and treatment increased cell viability (p˂0.001, p˂0.001) and reduce apoptosis (p˂0.001, p˂0.001) compared with the control group. (bakirkoymedj.org)
  • TTC, Nissl, and TUNEL staining showed the significant improvement of infarction volume, neuron morphology, and neuron apoptosis in rat with hydrogen treatment. (molecularhydrogenstudies.com)
  • Meanwhile, both MH and Ac-DEVD-CHO had similar effects in protecting cell morphology, reducing LDH release, and inhibiting OGD-induced apoptosis in neurons. (syksignal.com)
  • The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)
  • I focus my attention on ischemic/reperfusion injury to the brain. (benbest.com)
  • 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)
  • 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)
  • 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)
  • 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)
  • Contusions may lead to local edema and ischemia with resultant neurologic deterioration, increased intracranial pressure (ICP) and intracranial hypertension, and brain herniation. (medscape.com)
  • Most of the metabolic energy of neurons is expended on maintaining ion gradients across the cell membrane. (benbest.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)
  • Huwentoxin-I is known to be an inhibitor of tetrodotoxin -sensitive voltage-gated sodium channels (TTX-S) (IC 50 ~ 50 nM) and N-type voltage-sensitive calcium channels (IC 50 ~ 100 nM) in mammalian DRG, hippocampus and insect's DUM neurons. (smartox-biotech.com)
  • 2011 ) and inhibit neuronal apoptosis(Guo et al. (biomedcentral.com)
  • Huwentoxin-I (HWTX-I) is a 33-residue peptide isolated from the venom of Ornithoctonus huwena and could inhibit TTX-sensitive voltage-gated sodium channels and N-type calcium channels in mammalian dorsal root ganglion (DRG) neurons. (smartox-biotech.com)
  • Long-range monosynaptic inputs targeting apical and basal dendrites of primary motor cortex deep output neurons. (edu.hk)
  • 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)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
  • These findings suggest that neuronal apoptosis after cardiac arrest is not primarily initiated by activation of caspases. (asahq.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 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)