Oxidative / Nitrosative Stress in Rats Subjected to Focal Cerebral Ischemia / Reperfusion

Awooda, Hiba A.; Lutfi, Mohamed Faisal; G, Gihan M. Sharara; Saeed, Amal

doi:10.12816/0024679

Cited by 26 publications

(22 citation statements)

References 38 publications

(31 reference statements)

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“…The local accumulation of NO is also involved in the inflammatory cascade after cerebral ischemia [ 48 , 49 ]. This mediator enhances cell adhesion molecules expression on endothelial cells and promotes adhesion and transendothelial migration of immune cells [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Tuscan black kale sprout extract bioactivated with myrosinase: a novel natural product for neuroprotection by inflammatory and oxidative response during cerebral ischemia/reperfusion injury in rat

Giacoppo

Galuppo

Nicola

et al. 2015

BMC Complement Altern Med

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BackgroundCerebral ischemia and reperfusion (CIR) is a pathological condition characterized by a first blood supply restriction to brain followed by the consequent restoration of blood flow and simultaneous reoxygenation.The aim of this study was to evaluate the neuroprotective effects of Tuscan black kale sprout extract (TBK-SE) bioactivated with myrosinase enzyme, assessing its capability to preserve blood–brain barrier (BBB), in a rat model of CIR.MethodsCIR was induced in rats according to a classic model of carotid artery occlusion for a time period of 1 h and the reperfusion time was prolonged for seven days.ResultsBy immunohistochemical evaluation and western blot analysis of brain and cerebellum tissues, our data have clearly shown that administration of bioactive TBK-SE is able to restore alterations of tight junction components (claudin-5 immunolocalization). Also, bioactive TBK-SE reduces some inflammatory key-markers (p-selectin, GFAP, Iba-1, ERK1/2 and TNF-α), as well as the triggering of neuronal apoptotic death pathway (data about Bax/Bcl-2 balance, p53 and cleaved-caspase 3) and the generation of radicalic species by oxidative stress (results focused on iNOS, nitrotyrosine and Nrf2).ConclusionTaken together, our findings lead to believe that bioactive TBK-SE exerts pharmacological properties in protecting BBB integrity through a mechanism of action that involves a modulation of inflammatory and oxidative pathway as well into control of neuronal death.

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Section: Discussionmentioning

confidence: 99%

Tuscan black kale sprout extract bioactivated with myrosinase: a novel natural product for neuroprotection by inflammatory and oxidative response during cerebral ischemia/reperfusion injury in rat

Giacoppo

Galuppo

Nicola

et al. 2015

BMC Complement Altern Med

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“…Particularly, the brain is highly susceptible to free radical mediated insult owing to its high lipid content [21]. ROS levels are elevated in the cerebral vasculature during reperfusion period [22], and suspected to be an underlying cause of post-ischemic endothelial dysfunction, however, their enzymatic source(s) is yet to be defined [11]. The (nicotinamide adenine dinucleotide phosphate) NADPH oxidases are the only enzymes yet discovered with the primary function of generating superoxide and ROS in the cerebral vasculature under physiological conditions [23].…”

Section: Oxidative/nitrosative Stress In Cerebral Ischemiamentioning

confidence: 99%

“…Oxidative/nitrosative stresses are modulated by enzyme systems such as SOD and the nitric oxide synthase (NOS) family [25]. Mice with enhanced expression of SOD show reduced injury after cerebral ischemia, whereas those with a deficiency show increased injury, proving that excessive oxygen radical production is fundamental to ischemic brain injury, while in case of NOS activation during ischemia, superoxide reacts avidly with NO leading to decrease NO bioavailability and the formation of peroxynitrite a highly reactive and damaging species that causes nitration of tyrosine residues on proteins [11]…”

Section: Oxidative/nitrosative Stress In Cerebral Ischemiamentioning

confidence: 99%

“…There are many toxic aldehydes generated during lipid peroxidation: α, β unsaturated reactive aldehydes, such as malondialdehyde (MDA), 4-hydroxy-2nonenal (HNE), and 2-propenal (acrolein), and isoprostaness, 4-hydroxynonenal (4-HNE), which damages a variety of ion channels, transporter, and cytoskeletal proteins. These products of lipid peroxidation have therefore commonly been used as biomarkers of oxidative stress/damage [11] [22].…”

Section: Lipid Peroxidation and Malondialdehydementioning

confidence: 99%

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Pathophysiology of Cerebral Ischemia: Role of Oxidative/Nitrosative Stress

Awooda¹

2019

JBM

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Stroke is a devastating disease with a complex pathophysiology; it ranks second to ischemic heart disease as a cause of death and long-term disability. Tissue damage results from diverse mechanisms with central involvement of free radicals' overproduction that results in oxidative stress and hence contributes to brain damage. Free radicals [Reactive oxygen species/Reactive nitrogen species] play central a role in the diverse normal physiological processes and as defense mechanisms against harmful substances. When the rate of their production exceeds the antioxidant capacity of the body, oxidative stress occurs. Oxidative stress is implicated in the pathogenesis of various diseases including hypertension, atherosclerosis, diabetes mellitus and cancer; they mediate damage to cell structures, lipid peroxidation, protein denaturation, nucleic acid and DNA damage.

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“…It is characterized by an imbalance between the generation of reactive oxygen species (ROS) and the capacity of the intrinsic antioxidant defence system of the cerebral system [5]. In both experimental and clinical studies, this balance has shown increase in favour of oxidants in cases of transient ischaemia [6,7]. Several endogenous and exogenous antioxidants are used to neutralize and protect the brain from free radicals by maintaining the redox balance [8].…”

Section: Introductionmentioning

confidence: 99%

Oxidative injury associated with stenting of asymptomatic carotid artery stenosis

Saraçoğlu

Vuruşkan

Çekici

et al. 2017

Vasa

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Summary:Background: After carotid artery stenting (CAS), neurological complications that cannot be explained with imaging methods may develop. In our study we aimed to show, using oxidative stress markers, isolated oxidative damage and resulting neurological fi ndings following CAS in patients with asymptomatic carotid artery stenosis. Patients and methods: We included 131 neurologically asymptomatic patients requiring CAS. The neurological fi ndings were evaluated using the modifi ed Rankin Scale (mRS) prior to the procedure, one hour post-procedure, and two days after. Patients with elevated mRS scores but with or without typical hyperintense lesions observed on an MRI and with changes of oxidative stress marker levels at the time (Δtotal-thiol, Δtotal antioxidative status [TAS], and Δtotal oxidant status [TOS]) were evaluated. Results: In the neurological examination carried out one hour prior to the procedure, there were 92 patients with mRS = 0, 20 with mRS = 1, and 12 with mRS = 2. When Δtotal-thiol, ΔTAS, and ΔTOS values and the mRS were compared, it was observed that as the difference in oxidative parameters increased, clinical deterioration also increased proportionally (p = 0.001). Conclusions: We demonstrate a possible correlation between oxidative damage and neurological fi ndings after CAS which could not be explained by routine imaging methods. Keywords:Reperfusion injury, carotid artery stenting, oxidative damage, total thiol jor or minor thromboembolism by the imaging modalities after carotid artery stenting, might be the result of reperfusion injuries.Our research aimed at the underlying causes of the development of transient neurological complications that cannot be explained via imaging methods following elective CAS. We tried to show the isolated oxidative damage and the resulting clinical fi ndings following stenting in patients with asymptomatic carotid artery severe stenosis. Patients and methods Patient populationApproval for the study was received from our local ethical board. Between September 2014 and August 2016, we investigated a total of 343 consecutive severe carotid artery stenosis patients who are neurologically asymptomatic (without stroke, transient ischaemic attack or amaurosis fugax events within the previous six months). With the results of interdisciplinary consultation between the neurology and cardiovascular surgery departments, 160 patients were referred for carotid endarterectomy,

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Oxidative / Nitrosative Stress in Rats Subjected to Focal Cerebral Ischemia / Reperfusion

Abstract: Background: Ischemic stroke usually initiates inflammation and oxidative/nitrosative stress leading to neuronal death.

Cited by 26 publications

References 38 publications

Tuscan black kale sprout extract bioactivated with myrosinase: a novel natural product for neuroprotection by inflammatory and oxidative response during cerebral ischemia/reperfusion injury in rat

Tuscan black kale sprout extract bioactivated with myrosinase: a novel natural product for neuroprotection by inflammatory and oxidative response during cerebral ischemia/reperfusion injury in rat

Pathophysiology of Cerebral Ischemia: Role of Oxidative/Nitrosative Stress

Oxidative injury associated with stenting of asymptomatic carotid artery stenosis

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