scholarly journals Reactive Oxygen Species‐Responsive Nanoparticles for the Treatment of Ischemic Stroke

2019 ◽  
pp. 1900038 ◽  
Author(s):  
Olivera Rajkovic ◽  
Charlotte Gourmel ◽  
Richard d'Arcy ◽  
Raymond Wong ◽  
Ivana Rajkovic ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemic Stroke ◽  
Reactive Oxygen ◽  
Oxygen Species

Neural Stem Cells Transfected with Reactive Oxygen Species-Responsive Polyplexes for Effective Treatment of Ischemic Stroke

2019 ◽  
Vol 31 (10) ◽  
pp. 1807591 ◽  
Author(s):  
Xin-Chi Jiang ◽  
Jia-Jia Xiang ◽  
Hong-Hui Wu ◽  
Tian-Yuan Zhang ◽  
Dan-Ping Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Ischemic Stroke ◽  
Neural Stem Cells ◽  
Effective Treatment ◽  
Reactive Oxygen ◽  
Oxygen Species

Reactive oxygen species plasmatic levels in ischemic stroke

2007 ◽  
Vol 303 (1-2) ◽  
pp. 19-25 ◽  
Author(s):  
Laura Nanetti ◽  
Ruja Taffi ◽  
Arianna Vignini ◽  
Cinzia Moroni ◽  
Francesca Raffaelli ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemic Stroke ◽  
Reactive Oxygen ◽  
Oxygen Species

Improvement of a novel proposal for antioxidant treatment against brain damage occurring in ischemic stroke patients.

2020 ◽  
Vol 19 ◽  
Author(s):  
Sofía Orellana-Urzúa ◽  
Gonzalo Claps ◽  
Ramón Rodrigo
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemic Stroke ◽  
Experimental Studies ◽  
Reactive Oxygen ◽  
Cerebral Injury ◽  
Therapeutic Window ◽  
Oxygen Species ◽  
Iron Release ◽  
Stroke Patients

: The underlying mechanism of cerebral injury occurring in patients with acute ischemic stroke involves a key pathophysiological role of oxidative stress. Thus, reactive oxygen species are related to the development of brain edema, calcium overload, mitochondrial dysfunction, excitotoxicity, iron release and inflammation. Nevertheless, although experimental studies have tested the use of antioxidants as an adjuvant therapy in this setting, clinical data and randomized trials are still lacking. Current approved pharmacological therapy is aimed at reperfusion strategies; however, the therapeutic window is limited and also challenged by the injury known to result from the reperfusion. We have recently defined a timecourse occurrence of pathological events triggered by reperfusion-dependent increased reactive oxygen species, thus suggesting the beneficial role of the pertinent use of antioxidants. The present study was aimed to support the hypothesis that an enhanced antioxidant neuroprotection could be achieved by the use of two or more antioxidants opportunely provided to ischemic stroke patients focused against the specific mechanism occurring throughout the pathophysiological process. From this paradigm,using an underexplored therapeutic principle, it could be suggested that antioxidant-based therapy is a novel, promising, safe, available and cost-effective strategy against the deleterious effects of ischemic stroke that needs to be further studied in clinical protocols.

Leukocyte-Platelet Aggregates in Rat Peripheral Blood After Ischemic Stroke and Reperfusion

2005 ◽  
Vol 6 (4) ◽  
pp. 281-288 ◽  
Author(s):  
Leslie S. Ritter ◽  
Karl M. Stempel ◽  
Bruce M. Coull ◽  
Paul F. McDonagh
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemic Stroke ◽  
Adhesion Molecule ◽  
Peripheral Blood ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cd11b Expression ◽  
Platelet Aggregates ◽  
Species Production

Ischemic stroke and reperfusion (ISR) is associated with an inflammatory response characterized, in part, by the formation of leukocyte-platelet aggregates (LPA). Aggregate formation may amplify the immunologic and hemostatic functions of both cell types and thus exacerbate reperfusion injury after ischemic stroke. LPA formation in peripheral blood may also serve as a biomarker of the severity of injury. However, it is not fully known whether ISR causes LPA formation that can be detected in the peripheral blood. Therefore, the purpose of this study was to measure LPA in the peripheral blood after ISR using a rat model. The filament method was used to perform ISR. Blood was collected from the jugular vein before ischemia, after 4 hours of ischemia, and after 1 hour of reperfusion. Flow cytometry was used to quantify LPA in peripheral blood. Separate ISR groups were treated with tirofiban, a platelet GPIIb/IIIa inhibitor, and fucoidan, a selectin adhesion molecule inhibitor, and analyzed for LPA. Leukocyte CD11b expression and reactive oxygen species production were also analyzed to note the role of polymorphonuclear neutrophilic (PMN) activation on LPA formation. After ISR, LPA levels in peripheral blood were twice as large as preischemic levels. Both GPIIb/IIIa and selectin adhesion molecule inhibition (p < .05) decreased LPA to preischemic values. PMN CD11b expression was increased above baseline but did not differ between groups. Reactive oxygen species production did not differ between groups during reperfusion. These data suggest that ischemic stroke and reperfusion results in an increase in LPA that can be consistently measured in peripheral blood. LPA formation may be a useful biomarker and potential therapeutic target after ischemic stroke and reperfusion.

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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