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acetylcysteine/stroke
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Evidence for a Beneficial Effect of Oral N-acetylcysteine on Functional Outcomes and Inflammatory Biomarkers in Patients with Acute Ischemic Stroke
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Purpose: Numerous preclinical studies have demonstrated the potential neuroprotective effects of N-acetylcysteine (NAC) in the treatment of brain ischemia. Accordingly, the present study aimed to assess the potential therapeutic effects
Impact of N-Acetylcysteine on cerebral amyloid-β plaques and kidney damage in spontaneously hypertensive stroke-prone rats.
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BACKGROUND
Cerebral small vessel disease (CSVD) in spontaneously hypertensive stroke prone rats (SHRSP) is accompanied by parenchymal amyloid-β (Aβ) deposition in the brain and by hypertensive nephropathy with tubulointerstitial damage. N-acetylcysteine (NAC) promotes blood-brain barrier (BBB)
Administration of N-acetylcysteine after focal cerebral ischemia protects brain and reduces inflammation in a rat model of experimental stroke.
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Free radicals and inflammatory mediators are involved in transient focal cerebral ischemia (FCI). Preadministration of N-acetylcysteine (NAC) has been found to attenuate the cerebral ischemia-reperfusion injury in a rat model of experimental stroke. This study was undertaken to investigate the
The effect of ethyl pyruvate and N-acetylcysteine on ischemia-reperfusion injury in an experimental model of ischemic stroke.
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BACKGROUND
Reperfusion therapies play an important role in early-period treatment for patients presenting to the emergency department due to stroke. However, the ischemia-reperfusion injury that may occur with reperfusion must then be considered. The purpose of this study was to determine the
N-acetylcysteine targets 5 lipoxygenase-derived, toxic lipids and can synergize with prostaglandin E2 to inhibit ferroptosis and improve outcomes following hemorrhagic stroke in mice.
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OBJECTIVE
N-acetylcysteine (NAC) is a clinically approved thiol-containing redox modulatory compound currently in trials for many neurological and psychiatric disorders. Although generically labeled as an "antioxidant," poor understanding of its site(s) of action is a barrier to its use in
Effects of post-resuscitation treatment with N-acetylcysteine on cardiac recovery in hypoxic newborn piglets.
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OBJECTIVE
Although N-acetylcysteine (NAC) can decrease reactive oxygen species and improve myocardial recovery after ischemia/hypoxia in various acute animal models, little is known regarding its long-term effect in neonatal subjects. We investigated whether NAC provides prolonged protective effect
[EVALUATION OF NEUROPROTECTIVE ACTIVITY OF COMPLEX IMPACT OF MAGNESIUM OF SULFATE, LAMOTRYGINE AND N-ACETYLCYSTEINE UNDER CONDITIONS OF COMBINED NORMOBARIC HYPOXIA WITH LIGATION OF RIGHT CAROTID ARTERY IN RATS].
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Cerebrovascular diseases of ischemic origin still remain the leading cause of death and disability of the population. In acute cerebral discirculation conditions, anaerobic glycolysis is activated, ATP formation rate decreases, the ion pumps work is disrupted and superoxide radicals are formed.
Improvement in endothelial dysfunction in patients with systemic lupus erythematosus with N-acetylcysteine and atorvastatin.
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OBJECTIVE
To study the effects of N-acetylcysteine (NAC) and atorvastatin on endothelial dysfunction in patients with systemic lupus erythematosus (SLE).
METHODS
Thirty-two SLE patients and age, sex-matched 10 healthy control subjects were studied. The patients were between 17 and 65 years of age
N-acetylcysteine improves the hemodynamics and oxidative stress in hypoxic newborn pigs reoxygenated with 100% oxygen.
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Neonatal asphyxia may lead to cardiac and renal complications perhaps mediated by oxygen free radicals. Using a model of neonatal hypoxia-reoxygenation, we tested the hypothesis that N-acetylcysteine (NAC) would improve cardiac function and renal blood flow. Eighteen piglets (aged 1-4 days old,
Oral N-acetylcysteine and exercise tolerance in mild chronic obstructive pulmonary disease.
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Heightened oxidative stress is implicated in the progressive impairment of skeletal muscle vascular and mitochondrial function in chronic obstructive pulmonary disease (COPD). Whether accumulation of reactive oxygen species contributes to exercise intolerance in the early stages of COPD is unknown.
N-acetylcysteine infusion in viral myocarditis: a case report.
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N-acetylcysteine improves survival in established acute liver failure following paracetamol overdose by reducing the incidence of multiorgan failure. These benefits are thought to be related to decreased tissue hypoxia by the enhancement of both oxygen delivery and oxygen extraction. Similar
The antioxidant N-acetylcysteine preserves myocardial function and diminishes oxidative stress after cardioplegic arrest.
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OBJECTIVE
Oxidative stress contributes to myocardial ischemia-reperfusion injury. We hypothesized that administration of the antioxidant N-acetylcysteine would have beneficial effects on myocardial function after cardiopulmonary bypass and cardioplegic arrest.
METHODS
Anesthetized dogs (n = 18) were
The antioxidant acetylcysteine reduces cardiovascular events in patients with end-stage renal failure: a randomized, controlled trial.
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BACKGROUND
Patients with end-stage renal failure have increased oxidative stress and show elevated cardiovascular mortality. Whether increased cardiovascular events can be prevented by the administration of antioxidants is unknown.
RESULTS
We evaluated the effects of acetylcysteine, a
Cerebral glucose transporter: the possible therapeutic target for ischemic stroke.
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Hyperglycemia is considered to be associated with poor outcomes of ischemic stroke. However, it is controversial about the blood glucose-lowering therapy in patients with stroke. According to the current reports, hyperglycemia is an indicator of severe stroke and cannot increase cerebral glucose
The protection conferred against ischemia-reperfusion injury in the diabetic brain by N-acetylcysteine is associated with decreased dicarbonyl stress.
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Diabetes, a risk factor for stroke, leads to elevated blood methylglyoxal (MG) levels. This is due to increased MG generation from the high glucose levels, and because diabetes impairs the glutathione (GSH)-glyoxalase system for MG elimination. MG glycates proteins and causes dicarbonyl stress. We
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