Reactive oxygen species and ischemic cerebrovascular disease

Olmez, Inan; Özyurt, Hüseyın

doi:10.1016/j.neuint.2011.11.009

Cited by 258 publications

(187 citation statements)

References 73 publications

Supporting

Mentioning

175

Contrasting

Unclassified

Order By: Relevance

“…Surplus amount of ROS generation is thought to be the key module of neuronal damage in the brain. ROS can induce lipid peroxidation and disrupt the membrane lipid bilayer arrangement that may inactivate membrane-bound receptors and enzymes and increase tissue permeability (24,25). Products of lipid peroxidation, such as MDA and unsaturated aldehydes, are capable of inactivating many cellular proteins by forming protein crosslinkages (26).…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Ye¹,

Zhou²,

Wang³

et al. 2016

J Anesth Perioper Med

View full text Add to dashboard Cite

Background: Sevoflurane, as a novel volatile anesthetic with minimal pungency, low solubility, and less toxicity, is widely used in anesthetic practice. The purpose of this study was to investigate the effect of sevoflurane postconditioning on endogenous antioxidant status and spatial learning and memory ability after cardiac arrest (CA) and the potential underlying mechanisms. Methods: A rat model of CA was established by delivering an alternating current between the esophagus and chest wall to induce ventricular fibrillation. Animals were randomly divided into three groups: sham group (no CA), CA group, and CA + sevoflurane postconditioning (CA + SE) group. Sevoflurane postconditioning was achieved by administration of 2.5% sevoflurane for 60 min after resuscitation. The spatial learning and memory ability of rats was measured by the Morris water maze. The antioxidant enzymes activities were assessed at 4 hours, 1 day and 8 days after resuscitation. Moreover, the expressions of hippocampal proteins which could serve as memory enhancement biomarkers including growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD -95) and the transcription factor c-jun/activator protein-1 (AP-1), were detected at 8 days after resuscitation. Results: We found that CA significantly decreased the ability of spatial learning and memory in contrast to the sham controls. However, sevoflurane postconditioning significantly increased survival rate and antioxidant enzyme activities as well as ameliorated the spatial learning and memory deficits induced by CA. Furthermore, sevoflurane postconditioning regulated hippocampal memory enhancement proteins. Conclusions: Postconditioning with sevoflurane improved learning and memory deficits in a CA model possibly due to the reduction of oxidative stress and up-regulation of the memory enhancement biomarkers in hippocampus.

show abstract

Section: Discussionmentioning

confidence: 99%

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Ye¹,

Zhou²,

Wang³

et al. 2016

J Anesth Perioper Med

View full text Add to dashboard Cite

show abstract

“…Vascular apoptosis is triggered by pro-apoptotic factors and radical oxygen species (Fisher 2008;Olmez and Ozyurt 2012) resulting from oxidative stress during cerebral ischemia. Oxidative stress induces catalase and SOD-1 expression (Slemmer et al 2008;Facchinetti et al 1998) demonstrated here in the vessels of the ipsilateral hemisphere.…”

Section: Discussionmentioning

confidence: 99%

Neuropilin-1 modulates vascular endothelial growth factor-induced poly(ADP-ribose)-polymerase leading to reduced cerebrovascular apoptosis

Mey

Hörmann

Schleicher

et al. 2013

Neurobiology of Disease

View full text Add to dashboard Cite

Cerebral ischemia is encompassed by cerebrovascular apoptosis, yet the mechanisms behind apoptosis regulation are not fully understood. We previously demonstrated inhibition of endothelial apoptosis by vascular endothelial growth factor (VEGF) through upregulation of poly(ADP-ribose)-polymerase (PARP) expression. However, PARP overactivation through oxidative stress can lead to necrosis. This study tested the hypothesis that neuropilin-1 (NP-1), an alternative VEGF receptor, regulates the response to cerebral ischemia by modulating PARP expression and, in turn, apoptosis inhibition by VEGF. In endothelial cell culture, NP-1 colocalized with VEGF receptor-2 (VEGFR-2) and acted as its coreceptor. This significantly enhanced VEGF-induced PARP mRNA and protein expression demonstrated by receptor-specific inhibitors and VEGF-A isoforms. NP-1 augmented the inhibitory effect of VEGF/VEGFR-2 interaction on apoptosis induced by adhesion inhibition through the V-integrin inhibitor cRGDfV. NP-1/VEGFR-2 signal transduction involved JNK and Akt. In rat models of permanent and temporary middle cerebral artery occlusion, the ischemic cerebral hemispheres displayed endothelial and neuronal apoptosis next to increased endothelial NP-1 and VEGFR-2 expression compared to non-ischemic cerebral hemispheres, sham-operated or untreated controls. Increased vascular superoxide dismutase-1 and catalase expression as well as decreased glycogen reserves indicated oxidative stress in the ischemic brain. Of note, protein levels of intact PARP remained stable despite pro-apoptotic conditions through increased PARP mRNA production during cerebral ischemia. In conclusion, NP-1 is upregulated in conditions of imminent cerebrovascular apoptosis to reinforce apoptosis inhibition and modulate VEGF-dependent PARP expression and activation. We propose that NP-1 is a key modulator of VEGF maintaining cerebrovascular integrity during ischemia. Modulating the function of NP-1 to target PARP could help to prevent cellular damage in cerebrovascular disease.

show abstract

“…Free radical production can continue from the onset hours up to 21 days of permanent MCAO. Ischemic damage caused by free radical production, inhibits the antioxidant enzymes activities (20). Takagi et al (21) found that SOD activities of rat brain tissues was low markedly at 30 minutes, 4, 24 and 48 h after the permanent MCAO.…”

mentioning

confidence: 99%

Investigation of Epidermal Growth Factor, Tumor Necrosis Factor-alpha and Thioredoxin System in Rats Exposed to Cerebral Ischemia

Erol-Demirbilek

Kılıç

Kömürcü

2016

Revista Romana De Medicina De Laborator

View full text Add to dashboard Cite

show abstract

Reactive oxygen species and ischemic cerebrovascular disease

Cited by 258 publications

References 73 publications

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Neuropilin-1 modulates vascular endothelial growth factor-induced poly(ADP-ribose)-polymerase leading to reduced cerebrovascular apoptosis

Investigation of Epidermal Growth Factor, Tumor Necrosis Factor-alpha and Thioredoxin System in Rats Exposed to Cerebral Ischemia

Contact Info

Product

Resources

About