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nordihydroguaiaretic acid/инфаркт
Веза се чува у привремену меморију
8 резултати
[Nordihydroguaiaretic acid partially inhibits inflammatory responses after focal cerebral ischemia in rats].
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The aim of the present study is to investigate the role of nordihydroguaiaretic acid (NDGA) on inflammatory cells accumulation after focal cerebral ischemia and the underlying mechanism. Focal cerebral ischemia was induced by 30 min of middle cerebral artery occlusion (MCAO) followed by 72 h of
The protective effect of nordihydroguaiaretic acid on cerebral ischemia/reperfusion injury is mediated by the JNK pathway.
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Nordihydroguaiaretic acid (NDGA) is a powerful antioxidant and/or lipoxygenase (LOX) inhibitor which is isolated from Larrea tridentate. NDGA has been shown to have neuroprotective effects both in vitro and in vivo experiments. However, little is known regarding NDGA's protective mechanism in
Role of lipoxygenase metabolites in ischemic preconditioning.
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Preconditioning with brief intermittent periods of ischemia before a sustained period of ischemia has been shown to reduce infarct size and improve recovery of function in rat hearts. The mediators of this protective response are unknown in rats. We tested the hypothesis that a lipoxygenase
Lipid peroxidation, arachidonic acid and products of the lipoxygenase pathway in ischaemic preconditioning of rat heart.
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OBJECTIVE
Preconditioning with brief intermittent periods of ischaemia is known to provide protection against ischaemic injury. It has been suggested that myocardial ischaemia also activates phospholipase A2, which releases arachidonic acid from phospholipids. In the present study the possible role
Augmentation of leukotriene C4 and D4 release due to severe stenosis in the canine coronary artery stimulated by the calcium ionophore A23187.
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In dogs undergoing 24- or 72-hr severe narrowing of the left anterior descending coronary artery (LAD), the in vitro formation of immunoreactive leukotriene C4 (LTC4) by the stenosed LAD was greatly augmented by 1 microM A23187 in a 10-min incubation at 37 degrees. This stimulated LTC4 formation was
Effects of catecholamines on eicosanoid synthesis with special reference to prostanoid/leukotriene ratio.
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Catecholamines (adrenaline, dopamine, and noradrenaline) stimulate prostanoid synthesis by acting as "cosubstrates." On the other hand, many inhibitors of leukotriene synthesis, such as nordihydroguaiaretic acid and caffeic acid, have a catecholic structure. Catecholamines have opposite effects on
Calcium overload and cardiac myocyte cell damage induced by arachidonate lipoxygenation.
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The accumulation of arachidonic acid and lipoxygenase metabolites of arachidonate occurs in ischemic-reperfused myocardium. Although lipoxygenase inhibitors have been shown to attenuate myocardial infarct size after ischemia-reperfusion, the relationship between arachidonate lipoxygenation and
Protease-activated receptor 2 protects against myocardial ischemia-reperfusion injury through the lipoxygenase pathway and TRPV1 channels.
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This study tests the hypothesis that the lipoxygenase (LOX) pathway mediates protease-activated receptor (PAR) 2-induced activation of the transient receptor potential vanilloid receptor 1 (TRPV1) to protect the heart from ischemia/reperfusion (I/R) injury. SLIGRL, a PAR2 activating peptide, was
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