brain edema/protease

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Effects of focal mild hypothermia on thrombin-induced brain edema formation and the expression of protease activated receptor-1, matrix metalloproteinase-9 and aquaporin 4 in rats.

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Hypothermia is an effective neuroprotective treatment for brain injury caused by intracerebral hemorrhage (ICH). It is reported to reduce brain edema and neuronal cell death. Thrombin, a coagulation protease released from blood clots, is critical in brain edema formation following ICH. Protease

The expression and the role of protease nexin-1 on brain edema after intracerebral hemorrhage.

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Brain edema is one of the most frequent and serious complications of intracerebral hemorrhage (ICH), but how the ICH cause brain edema is unknown. Our studies were designed to investigate the regulation and distribution of protease nexin-1 (PN-1), thrombin and aquaporin-4 (AQP-4) in brain edema

Protease activated receptor-1 and brain edema formation in glioma models.

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OBJECTIVE Our previous studies showed that thrombin contributes to brain edema in gliomas. The present study investigated the role of a thrombin receptor, protease activated receptor-1 (PAR-1), in edema formation in glioma models. METHODS These experiments were performed in Fischer 344 rats, PAR-1

Protease-activated receptor 1 inhibitor improves brain edema in rats with intracerebral hemorrhage

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Aim: To investigate the changes of water content in brain tissue, the expression of AQP4mRNA after cerebral hemorrhage in rats, and the intervention effect of Protease activated receptor 1 inhibitor (PAR1 inhibitor) on both.

[Effect of agents increasing the resistance of the vascular wall as well as of trasylol (a protease inhibitor) on experimental brain edema].

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"Effects of baicalin on protease-activated receptor-1 expression and brain injury in a rat model of intracerebral hemorrhage".

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"Baicalin, a major flavonoid compound isolated from the dry roots of Scutellaria baicalensis Georgi, has been shown to be neuroprotective after ischemic brain injury. However, little is known about its effects on brain injury following intracerebral hemorrhage (ICH). In this study, we evaluated the

Induction of colligin may attenuate brain edema following intracerebral hemorrhage.

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Brain edema plays an important role in the secondary brain injury following intracerebral hemorrhage (ICH). Edema formation after ICH has been linked to thrombin toxicity. Therefore, the induction of endogenous serine protease inhibitors, which inhibit thrombin prior to ICH may limit edema

Ischaemic brain oedema.

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Ischaemic brain oedema appears to involve two distinct processes, the relative contribution and time course of which depend on the duration and severity of ischaemia, and the presence of reperfusion. The first process involves an increase in tissue Na+ and water content accompanying increased

Brain protease activity after experimental head injury.

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In an experimental series on twelve cats, activity changes of brain cell proteolytic activity were measured two hours after a blunt head injury without hematoma or contusions. Protease activity was estimated in two different brain tissue homogenate supernatants containing total soluble and only

Changes of perivascular macrophages in the process of brain edema induced by cold injury.

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Perivascular macrophages are considered as cerebral scavenger cells under physical and pathological conditions. In this study, we tried to examine changes of perivascular macrophages, especially changes of the characteristic lysosomal inclusion bodies that are rich in hydrolytic enzymes, in the

Serine protease inhibitor attenuates intracerebral hemorrhage-induced brain injury and edema formation in rat.

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Our previous studies have demonstrated that thrombin plays an important role in intracerebral hemorrhage (ICH)-induced brain injury and edema formation. We, therefore, examined whether nafamostat mesilate (FUT), a serine protease inhibitor, can reduce ICH-induced brain injury. Anesthetized male

Thrombin-induced tolerance against oxygen-glucose deprivation in astrocytes: role of protease-activated receptor-1.

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Our previous studies have found that pretreatment with a low dose of thrombin (thrombin preconditioning, TPC) reduces infarct volume and attenuates brain edema after focal cerebral ischemia in vivo and protects against the neuronal death induced by oxygen glucose deprivation (OGD) in vitro. In this

[Host cellular proteases trigger the infectivity of the influenza virus in the airway and brain].

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The pathogenesis of the influenza and Sendai viruses is primarily determined by host cellular trypsin-type processing proteases that activate viral fusion activity and infectivity. We isolated three secretory trypsin-type proteases from rat lungs, such as tryptase Clara, mini-plasmin, and ectopic

[Effect of baicalin on protease-activated receptor-1 expression and cell apoptosis in brain of rat with intracerebral hemorrhage].

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OBJECTIVE To investigate the protective effect and mechanism of baicalin on nerve tissue in rat with intracerebral hemorrhage (ICH). METHODS Rats were randomly divided into five groups: the sham-operated group, the ICH model group, and the three baicalin treated groups treated respectively with

[A contribution to the pathophysiology of post-traumatic brain oedema (author's transl)].

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The aim of this paper is to contrast new results obtained on the activities of lysosomal proteases in the brain of traumatized animals with the previously held opinions concerning the development of post-traumatic brain oedema. Two hours after a standardized head injury in the cat, acid and neutral

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