Correlation of Oxidative Stress Parameters and Inflammatory Markers in Ischemic Stroke Patients

Chehaibi, Khouloud; Trabelsi, Imen; Mahdouani, Kacem; Slimane, Mohamed Naceur

doi:10.1016/j.jstrokecerebrovasdis.2016.06.042

Cited by 57 publications

(40 citation statements)

References 64 publications

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“…It has been reported that oxidative stress–induced adult NSC apoptosis plays a critical role in the pathogenesis of ischemic stroke and its complications (Chehaibi et al, ; Yamauchi et al, ). Oxidative stress is a primary factor that has been shown to affect adult NSC function, differentiation, and survival (Wang, Liu, et al, ).…”

Section: Resultsmentioning

confidence: 99%

“…The mechanisms underlying the protective effect of the mfat‐1 transgene against hypoxic damage to adult NSCs from CoCl 2 are still not fully understood. Previous studies have reported that oxidative stress–induced neuronal apoptosis plays an important role in the pathogenesis of ischemic stroke (Chehaibi et al, ; Yamauchi et al, ). Recent investigations have indicated that overproduction of n‐3 PUFAs is highly effective in protecting the brain, and that there are protective mechanisms involved in Nrf2 activation and HO‐1 upregulation (Zhang et al, ).…”

Section: Discussionmentioning

confidence: 99%

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mfat‐1 transgene protects cultured adult neural stem cells against cobalt chloride‐mediated hypoxic injury by activating Nrf2/ARE pathways

Yang

Fang

et al. 2017

J of Neuroscience Research

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Ischemic stroke is a devastating neurological disorder and one of the leading causes of death and serious disability in adults. Adult neural stem cell (NSC) replacement therapy is a promising treatment for both structural and functional neurological recovery. However, for the treatment to work, adult NSCs must be protected against hypoxic-ischemic damage in the ischemic penumbra. In the present study, we aimed to investigate the neuroprotective effects of the mfat-1 transgene on cobalt chloride (CoCl 2 )-induced hypoxic-ischemic injury in cultured adult NSCs as well as its underlying mechanisms. The results show that in the CoCl 2 -induced hypoxic-ischemic injury model, the mfat-1 transgene enhanced the viability of adult NSCs and suppressed CoCl 2 -mediated apoptosis of adult NSCs. Additionally, the mfat-1 transgene promoted the proliferation of NSCs as shown by increased bromodeoxyuridine labeling of adult NSCs. This process was related to the reduction of reactive oxygen species. Quantitative real-time polymerase chain reaction and Western blot analysis revealed a much higher expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream genes (HO-1, NQO-1, GCLC). Taken together, our findings show that the mfat-1 transgene restored the CoCl 2 -inhibited viability and proliferation of NSCs by activating nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response elements (ARE) signal pathway to inhibit oxidative stress injury.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mfat‐1 transgene protects cultured adult neural stem cells against cobalt chloride‐mediated hypoxic injury by activating Nrf2/ARE pathways

Yang

Fang

et al. 2017

J of Neuroscience Research

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“…In this study, the antioxidants examined were thiol, an organic antioxidant containing a sulphydryl (-SH) group with a critical role in preventing oxidative stress in the cells, and total antioxidant status (TAS) levels, including endogenous antioxidants [11,12]. Oxidants were measured using a total oxidant status (TOS) kit that included diff erent oxidant molecules in the total measurement [13].…”

Section: Measurement Of Antioxidant and Oxidant Levelsmentioning

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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“…Redox disequilibrium, disruption of ionic homeostasis, lactic acidosis and defects in neurotransmitter metabolism are critical aspects of cerebral ischaemia/reperfusion injury. They are associated with broader, well-defined events in stroke pathophysiology, such as excitotoxicity and inflammation, and present targets for neuroprotection [7-12]. …”

Section: Introductionmentioning

confidence: 99%

Improvement of 2-Vessel Occlusion Cerebral Ischaemia/Reperfusion-Induced Corticostriatal Electrolyte and Redox Imbalance, Lactic Acidosis and Modified Acetylcholinesterase Activity by Kolaviron Correlates with Reduction in Neurobehavioural Deficits

et al. 2017

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Background: Disruption of electrolyte, redox and neurochemical homeostasis alongside cellular energy crisis is a hallmark of cerebral ischaemia and reperfusion injury. Purpose: This study investigated the effect of kolaviron (KV) on cortical and striatal cation imbalance, oxidative stress and neurochemical disturbances as well as neurobehavioural deficits in animals subjected to bilateral common carotid artery occlusion (BCCAO)-induced ischaemia/reperfusion injury. Methods: KV was administered at a dose of 100 or 200 mg/kg to male Wistar rats 1 h before a 30 min BCCAO/4 h reperfusion (I/R). This was followed by neurobehavioral assessment and biochemical evaluations of cation levels, oxidative stress indicators, lactate dehydrogenase activity and acetylcholinesterase (AChE) activity in the brain of animals. Conclusion: KV significantly restored altered cortical and striatal Ca²⁺, Na⁺, K⁺ and Mg²⁺ levels, ameliorated redox imbalance, lactic acidosis and modified AChE activity caused by I/R injury. The favourable neurobehavioural effects of KV correlated with biochemical outcomes. The pharmacological potential of KV in the treatment and management of ischemic stroke and allied pathological conditions via multiple targets (neurotransmitter metabolism, bioenergetic failure and ionic homeostasis) is highlighted by the study.

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Correlation of Oxidative Stress Parameters and Inflammatory Markers in Ischemic Stroke Patients

Cited by 57 publications

References 64 publications

mfat‐1 transgene protects cultured adult neural stem cells against cobalt chloride‐mediated hypoxic injury by activating Nrf2/ARE pathways

mfat‐1 transgene protects cultured adult neural stem cells against cobalt chloride‐mediated hypoxic injury by activating Nrf2/ARE pathways

Oxidative injury associated with stenting of asymptomatic carotid artery stenosis

Improvement of 2-Vessel Occlusion Cerebral Ischaemia/Reperfusion-Induced Corticostriatal Electrolyte and Redox Imbalance, Lactic Acidosis and Modified Acetylcholinesterase Activity by Kolaviron Correlates with Reduction in Neurobehavioural Deficits

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