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Página 1 a partir de 44 resultados
Spermine reduces infarction and neurological deficit following a rat model of middle cerebral artery occlusion: a magnetic resonance imaging study.
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The role of nitric oxide (NO) in post-ischemic cerebral infarction has been extensively examined, but few studies have investigated its role on the neurological deficit. In the present study, we investigated the effect of spermine on the temporal evolution of infarct volume, NO production and
Reduction of infarct size by the NO donors sodium nitroprusside and spermine/NO after transient focal cerebral ischemia in rats.
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Nitric oxide (NO) plays a dual role (neuroprotection and neurotoxicity) in cerebral ischemia. NO promoting strategies may be beneficial shortly after ischemia. Therefore, we have studied the hemodynamic and possible neuroprotective effects of two NO donors, the classical nitrovasodilator sodium
Spermidine/spermine-N¹-acetyltransferase in kidney ischemia reperfusion injury.
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Ischemic reperfusion injuries such as acute renal failure, acute liver failure, stroke, and myocardial infarction are prevalent causes of morbidity and mortality. Kidney ischemic reperfusion injury is the leading cause of acute renal failure and dysfunction of transplanted kidneys. Although
Exogenous spermine reduces ischemic damage in a model of focal cerebral ischemia in the rat.
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Alterations in polyamine metabolism during and after global or focal cerebral ischemia can produce a multiplicity of effects on brain such as modification in mitochondria calcium buffering capacity, exacerbating glutamate-mediated neurotoxicity, and impairment of the blood-brain barrier. In this
Transplantation of genetically engineered mesenchymal stem cells improves cardiac function in rats with myocardial infarction: benefit of a novel nonviral vector, cationized dextran.
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It is expected that mesenchymal stem cells (MSCs) will be a cell source for cardiac reconstruction because of their differentiation potential and ability to supply growth factors. However, poor viability at the transplanted site often hinders the therapeutic potential of MSCs. Here, in a trial
The effect of mitochondrial calcium uniporter opener spermine on diazoxide against focal cerebral ischemia--reperfusion injury in rats.
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BACKGROUND
Recent research has indicated that mitochondrial adenosine triphosphate-sensitive potassium channels play an important role in cerebral protection, which involves in attenuating the calcium of mitochondria. However, the effect of diazoxide on cerebral ischemia-reperfusion and the role of
Abnormal vasoconstrictor responses to angiotensin II and noradrenaline in isolated small arteries from patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
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OBJECTIVE
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is characterized by ultrastructural abnormalities in small cerebral and systemic vessels. We assessed vasomotor function in systemic small arteries in CADASIL.
METHODS
We studied 10 CADASIL
Spermine attenuates the preconditioning of diazoxide against transient focal cerebral ischemia in rats.
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It is known that mitochondrial ATP-sensitive potassium channels (mitoKATP) play a significant role in protecting cerebral function from ischemia-reperfusion injury, which is related with a decrease in the mitochondrial matrix calcium. However, the effect of mitochondrial calcium uniporter (MCU) on
Aggravation of brain infarction through an increase in acrolein production and a decrease in glutathione with aging.
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We previously reported that tissue damage during brain infarction was mainly caused by inactivation of proteins by acrolein. This time, it was tested why brain infarction increases in parallel with aging. A mouse model of photochemically induced thrombosis (PIT) was studied using 2, 6, and 12
Mitochondrial calcium uniporter opener spermine attenuates the cerebral protection of diazoxide through apoptosis in rats.
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BACKGROUND
It is reported that ischemic penumbra is a dynamic process, in which irreversible necrosis in the center of ischemia propagates to the neighboring tissue over time. Recent research has indicated that mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels (mitoKATP) opener
N1-Nonyl-1,4-diaminobutane ameliorates brain infarction size in photochemically induced thrombosis model mice.
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Inhibitors for polyamine oxidizing enzymes, spermine oxidase (SMOX) and N1-acetylpolyamine oxidase (PAOX), were designed and evaluated for their effectiveness in a photochemically induced thrombosis (PIT) mouse model. N1-Nonyl-1,4-diaminobutane (C9-4) and N1-tridecyl-1,4-diaminobutane (C13-4)
Acrolein, IL-6 and CRP as markers of silent brain infarction.
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We found previously that increased levels of polyamine oxidase (PAO) [acetylpolyamine oxidase (AcPAO) plus spermine oxidase (SMO)], and acrolein (CH(2)CHCHO) are good markers of stroke. We then investigated whether silent brain infarction (SBI) can be detected by measuring acrolein, PAO, or other
Differing effects of alpha-difluoromethylornithine and CGP 40116 on polyamine levels and infarct volume in a rat model of focal cerebral ischaemia.
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Focal cerebral ischaemia was induced in rats by occlusion of the left middle cerebral artery. Two days later, infarct volume was determined by magnetic resonance imaging and the concentrations of the polyamines putrescine (PU), spermine and spermidine by HPLC. In control (occluded) animals, PU
Spermine ameliorates ischemia/reperfusion injury in cardiomyocytes via regulation of autophagy.
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Myocardial infarction could result in high morbidity and mortality and heart diseases of children have becoming prevalent. Functions of spermine administration on cardiomyocytes remain unknown. The present study was designed to investigate the role of spermine pretreatment on myocardial
Neuroprotective effects of spermine following hypoxic-ischemic-induced brain damage: a mechanistic study.
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The polyamines (spermine, putrescine, and spermidine) can have neurotoxic or neuroprotective properties in models of neurodegeneration. However, assessment in a model of hypoxia-ischemia (HI) has not been defined. Furthermore, the putative mechanisms of neuroprotection have not been elucidated.
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