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pyrrolidine/krvarenje
Veza se sprema u međuspremnik
Stranica 1 iz 33 rezultatima
Pyrrolidine dithiocarbamate modulates HSP70, iNOS, and apoptosis during hemorrhagic shock resuscitation in rats.
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BACKGROUND
The aim of this study is to evaluate whether hemorrhage and resuscitation affect liver, intestinal, and renal expressions of heat shock protein 70 (HSP70), inducible nitric oxide synthase (iNOS), and apoptosis indexes (TUNEL, caspase-3 activation) and whether the expression of these
Effects of dimethyl sulfoxide, pyrrolidine dithiocarbamate, and methylprednisolone on nuclear factor-kappaB and heat shock protein 70 in a rat model of hemorrhagic shock.
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BACKGROUND
Nuclear factor kappa B (NF-kappaB) is a transcription factor involved in the inflammatory response. Heat shock protein 70 (HSP70) is involved in the cell protection from various stresses. The aim of this study was to evaluate the effects of dimethyl sulfoxide (DMSO), pyrrolidine
Pyrrolidine dithiocarbamate improves mortality in a rat model of severe hemorrhage.
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BACKGROUND
Hemorrhagic shock is a life threatening condition characterized by diminishing organ function. The aim of this study was to determine whether an effective pyrrolidine dithiocarbamate (PDTC) treatment protocol could be established to decrease organ dysfunction and mortality in a lethal
Pyrrolidine dithiocarbamate reduces the severity of cerulein-induced murine acute pancreatitis.
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The nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays a pivotal role in the induction of genes involved in the response to injury and inflammation. Dithiocarbamates are antioxidants that are potent inhibitors of NF-kappaB. This study tested the hypothesis that pyrrolidine
Organ-Specific Oxidative Events under Restrictive Versus Full Reperfusion Following Hemorrhagic Traumatic Shock in Rats.
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Background aim: Reperfusion after hemorrhagic traumatic shock (HTS) is often associated with complications that are partly ascribed to the formation of reactive oxygen species (ROS). The aim of our study was to compare the effects of restrictive reperfusion (RR) to rapid full reperfusion (FR) on ROS
Reactive nitrogen species inhibit alveolar epithelial fluid transport after hemorrhagic shock in rats.
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Our recent experimental work demonstrated that a neutrophil-dependent inflammatory response in the lung prevented the normal up-regulation of alveolar fluid clearance by catecholamines following hemorrhagic shock. In this study, we tested the hypothesis that the release of NO within the airspaces of
Rons formation under restrictive reperfusion does not affect organ dysfunction early after hemorrhage and trauma.
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Reactive oxygen species have been implicated in the pathophysiology of early reperfusion. We aimed to determine 1) reactive oxygen and nitrogen species (RONS) formation in organs of rats and 2) its pathophysiological relevance during a phase of restrictive reperfusion after hemorrhagic/traumatic
Potential contribution of nuclear factor-kappaB to cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.
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Nuclear factor-kappaB (NF-kappaB) plays a key role in inflammation, which is involved in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study, we assessed the potential role of NF-kappaB in regulation of cerebral vasospasm. Nuclear factor-kappaB DNA-binding
Pyrrolidine dithiocarbamate attenuates the development of monocrotaline-induced pulmonary arterial hypertension.
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We aimed to demonstrate the potential protective effects of pyrrolidine dithiocarbamate (PDTC) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Adult male rats were randomly assigned to 4 groups: control group, MCT-treated rats only, MCT-injected rats treated with PDTC, and
Pyrrolidine dithiocarbamate attenuates alcohol-induced leukocyte-endothelial cell interaction and cerebral vascular damage in rats: possible role of activation of transcription factor NF-kappaB in alcohol brain pathology.
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Effects of chronic (14-day) pretreatment of orally administered pyrrolidine dithiocarbamate (PDTC) (100 or 200 mg/kg/day) on alcohol-induced venular cerebrovasospasm, microvessel rupture, leukocyte-endothelial chemoattraction, and microhemorrhaging was studied by direct, quantitative in vivo
Early administration of pyrrolidine dithiocarbamate extends the therapeutic time window of tissue plasminogen activator in a male rat model of embolic stroke.
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Tissue plasminogen activator (tPA) is used in fewer than 4% of patients after ischemic stroke because of its narrow therapeutic time window. We tested whether pyrrolidine dithiocarbamate (PDTC), a drug with multiple mechanisms to provide neuroprotection, can be used to extend the therapeutic time
Activation of nuclear factor-kappa B and effects of pyrrolidine dithiocarbamate on TNBS-induced rat colitis.
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OBJECTIVE
To explore the changes of nuclear factor-kappa B (NF-kappaB) DNA-binding activity, the expression of intercellular adhesion molecule-1 (ICAM-1) regulated by NF-kappaB at various times and to evaluate the effects of pyrrolidine dithiocarbamate (PDTC) on trinitrobenzene sulfonic acid
Structure-based drug design of pyrrolidine-1, 2-dicarboxamides as a novel series of orally bioavailable factor Xa inhibitors.
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A novel series of pyrrolidine-1,2-dicarboxamides was discovered as factor Xa inhibitors using structure-based drug design. This series consisted of a neutral 4-chlorophenylurea P1, a biphenylsulfonamide P4 and a D-proline scaffold (1, IC(50) = 18 nM). Optimization of the initial hit resulted in an
Potential dual role of nuclear factor-kappa B in experimental subarachnoid hemorrhage-induced early brain injury in rabbits.
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OBJECTIVE
Nuclear factor-kappa B (NF-κB) has multiple physiological and pathological functions. The role of NF-κB can be protective or destructive. We aim to investigate the biphasic activation of NF-κB in brain after subarachnoid hemorrhage (SAH).
METHODS
Eighty male New Zealand rabbits are
Protective effect of pyrrolidine dithiocarbamate on liver injury induced by intestinal ischemia-reperfusion in rats.
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BACKGROUND
The nuclear translocation of transcription factors may be a critical factor in the intracellular pathway involved in ischemia/reperfusion (I/R) injury. The aim of the study was to evaluate the role of nuclear factor-kappa B (NF-kappaB) in the pathogenesis of liver injury induced by
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