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superoxide dismutase/stroke
Länken sparas på Urklipp
Sida 1 från 638 resultat
Angiotensin II type 1 receptor antagonist and angiotensin-converting enzyme inhibitor altered the activation of Cu/Zn-containing superoxide dismutase in the heart of stroke-prone spontaneously hypertensive rats.
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Although angiotensin II type 1 (AT1) receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors are known to reduce both reactive oxygen species (ROS) generated by activated NAD(P)H oxidase and vascular remodeling in hypertension, the effects of AT1 receptor antagonists or ACE
Chronic treatment with a superoxide dismutase mimetic prevents vascular remodeling and progression of hypertension in salt-loaded stroke-prone spontaneously hypertensive rats.
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Oxidative stress has been implicated in the pathogenesis of hypertension. The aim of the present study was to determine whether increased generation of vascular superoxide anion (*O2-) contributes to blood pressure elevation by influencing vascular function and structure in severely hypertensive
Brain-Derived Neurotrophic Factor Levels are Lower in Chronic Stroke Patients: A Relation with Manganese-dependent Superoxide Dismutase ALA16VAL Single Nucleotide Polymorphism through Tumor Necrosis Factor-α and Caspases Pathways.
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The manganese-dependent superoxide dismutase (MnSOD) Ala16Val single nucleotide polymorphism (SNP) has shown to be associated to risk factors of vascular diseases. Brain-Derived Neurotrophic Factor (BDNF) plays an essential role in the plasticity and neuronal regeneration of the brain after vascular
Superoxide dismutase mimetic, tempol, aggravates renal injury in advanced-stage stroke-prone spontaneously hypertensive rats.
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OBJECTIVE
The aim of this study was to determine whether antioxidant therapy could relieve hypertension and retard the progression of renal damage in advanced-stage hypertensive rats.
METHODS
Twenty-four-week-old spontaneously hypertensive stroke-prone rats were treated for 8 weeks with the
Kinetics differ between copper-zinc and manganese superoxide dismutase activity with acute ischemic stroke.
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This study aimed to clarify the kinetics of copper-zinc (CuZn) and manganese (Mn) superoxide dismutase (SOD) activity in acute ischemic stroke victims. Using the nitrite method, we investigated sequential changes in CuZn and Mn SOD activity in the cerebrospinal fluid (CSF) of 8 patients with acute
Regional distribution of superoxide dismutase in the brain and myocardium of the stroke-prone spontaneously hypertensive rat.
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1. Enzyme activities and contents of manganese and copper-zinc superoxide dismutase (Mn-, Cu/Zn-SOD) and oxygen free-radical scavengers were determined in the myocardium (right, left ventricle) and brain (cerebral cortex, hippocampus) of 15 and 31 week old stroke-prone spontaneously hypertensive
Acute-phase serum superoxide dismutase level as a predictive biomarker for stroke-associated infection.
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Background and Purpose: Oxidative stress is involved in the development of infections. However, whether oxidative stress indicators can be used as markers of stroke-associated infection (SAI) is still unclear. The purpose of this study was to test the predictive values of superoxide dismutase
The effect of superoxide dismutase enzyme inhibition on renal microcirculation of spontaneously hypertensive-stroke prone and Wistar rats.
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A significant factor in the development of hypertension may be excessive vasoconstriction within the renal medulla. This study therefore investigated the role of superoxide dismutase (SOD) in the regulation of renal medullary and cortical blood perfusion (MBP and CBP, respectively) in both
Antioxidant effects of vitamins C and E are associated with altered activation of vascular NADPH oxidase and superoxide dismutase in stroke-prone SHR.
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Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have antioxidant properties that could improve redox-sensitive vascular changes associated with hypertension. We determined whether vitamins C and E influence vascular function and structure in hypertension by modulating activity of NADPH
Sympathoinhibition induced by centrally administered atorvastatin is associated with alteration of NAD(P)H and Mn superoxide dismutase activity in rostral ventrolateral medulla of stroke-prone spontaneously hypertensive rats.
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Oxidative stress in the rostral ventrolateral medulla (RVLM) increases sympathetic nervous system activity (SNA). Oral treatment with atorvastatin decreases SNA through antioxidant effects in the RVLM of stroke-prone spontaneously hypertensive rats (SHRSP). We aimed to examine whether centrally
Calcium antagonist reduces oxidative stress by upregulating Cu/Zn superoxide dismutase in stroke-prone spontaneously hypertensive rats.
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Recent studies have suggested that the calcium antagonists have an antiatherogenic antioxidant property. The effects of the calcium antagonists on reactive oxygen species (ROS)-related enzymes, however, remain unknown. We hypothesized that the calcium antagonists inhibit oxidative stress in the
Uric acid and Cu/Zn superoxide dismutase: potential strategies and biomarkers in functional recovery of post-acute ischemic stroke patients after intensive neurorehabilitation.
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No evidence is currently provided on the involvement of uric acid (UA) and Cu/Zn Superoxide Dismutase (Cu/Zn SOD) in functional recovery of stroke patients after neurorehabilitation. For this purpose, the relationship between UA and Cu/Zn SOD plasma levels and clinical and functional outcome
Increase in superoxide dismutase after cerebrovascular accident.
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Superoxide dismutase (SOD), neuron specific enolase (NSE) and lactic dehydrogenase (LDH) were measured in the serum and cerebrospinal fluid (CSF) of ischemic cerebrovascular patients, other neurological patients and in age-matched healthy controls (serum only). The levels of SOD in the CSF or serum
Neuroprotection by manganese superoxide dismutase (MnSOD) mimics: antioxidant effect and oxidative stress regulation in acute experimental stroke.
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OBJECTIVE
Manganese superoxide dismutase (MnSOD), one of the most crucial antioxidant enzymes in the central nervous system, is thought to be one of the major mechanisms by which cells counteract the injuries of reactive oxygen species after cerebral ischemia. In this study, we used a novel
Synthetic combined superoxide dismutase/catalase mimetics are protective as a delayed treatment in a rat stroke model: a key role for reactive oxygen species in ischemic brain injury.
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Stroke is a severe and prevalent syndrome for which there is a great need for treatment, including agents to block the cascade of brain injury that occurs in the hours after the onset of ischemia. Reactive oxygen species (ROS) have been implicated in this destructive process, but antioxidant enzymes
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