anthranilic acid/stroke

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3-hydroxi-anthranilic acid is early expressed in stroke.

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Using an immunohistochemical technique, we have studied the distribution of 3-OH-anthranilic acid (3-HAA) in the rat brain. Our study was carried out in control animals and in rats in which a stroke model (single transient middle cerebral artery occlusion) was performed. A monoclonal antibody

Gemst: a taylor-made combination that reverts neuroanatomical changes in stroke.

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In a single transient middle cerebral artery occlusion model of stroke and using immunohistochemical techniques, the effects of a new therapeutic approach named Gemst (a member of the Poly-L-Lysine innovative therapies) have been studied in the rat brain. The expression of inflammatory (CD45,

Transient receptor potential melastatin subfamily member 2 cation channel regulates detrimental immune cell invasion in ischemic stroke.

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OBJECTIVE Brain injury during stroke results in oxidative stress and the release of factors that include extracellular Ca(2+), hydrogen peroxide, adenosine diphosphate ribose, and nicotinic acid adenine dinucleotide phosphate. These alterations of the extracellular milieu change the activity of

On the Biological Importance of the 3-hydroxyanthranilic Acid: Anthranilic Acid Ratio.

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Of the major components of the kynurenine pathway for the oxidative metabolism of tryptophan, most attention has focussed on the N-methyl-D-aspartate (NMDA) receptor agonist quinolinic acid, and the glutamate receptor blocker kynurenic acid. However, there is increasing evidence that the

Altered kynurenine metabolism correlates with infarct volume in stroke.

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Inflammation and oxidative stress are involved in brain damage following stroke, and tryptophan oxidation along the kynurenine pathway contributes to the modulation of oxidative stress partly via the glutamate receptor agonist quinolinic acid and antagonist kynurenic acid, and via redox-active

Tryptophan Metabolism, Inflammation, and Oxidative Stress in Patients With Neurovascular Disease

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Atherosclerosis is a leading cause of major vascular events, myocardial infarction, and ischemic stroke. Tryptophan (TRP) catabolism was recognized as an important player in inflammation and immune response having together with oxidative stress (OS) significant effects on each phase of

Electrochemical and in vitro evaluation of the redox-properties of kynurenine species.

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Kynurenines are formed as part of the tryptophan metabolism and are known to exhibit pro- and anti-oxidant activities in vitro. The mapping of these biological redox-systems and identification of potential in vivo targets are therefore of great interest in cellular physiology. Here the

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