Aryl hydrocarbon receptor modulates stroke-induced astrogliosis and neurogenesis in the adult mouse brain.

Background: The aryl hydrocarbon receptor (AHR) is a ligand-dependent transcription factor activated by environmental agonists and dietary tryptophan metabolites for the immune response and cell cycle regulation. Emerging evidence suggests that AHR activation after acute stroke may play a role in brain ischemic injury. However, whether AHR activation alters poststroke astrogliosis and neurogenesis remains unknown.

Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation.

Inhibition and deletion of soluble epoxide hydrolase (sEH) has been suggested to ameliorate infarction in experimental ischemic stroke possibly via vasoactive epoxyeicosatrienoic acids. However, it is unknown whether the neuroprotective mechanisms involve alteration of post-ischemic neuronal transmission and neurotrophic signaling. We used a permanent middle cerebral artery occlusion (MCAO) model in adult wild-type mice with the sEH inhibitor 12-(3-adamantan-1-yl-ureido)dodecanoic acid (AUDA) post-treatment and in sEH knockout (sEH KO) mice.

Resveratrol reduces infarct size and improves ventricular function after myocardial ischemia in rats.

The purpose of this study was to investigate the effect of resveratrol, a polyphenol present in grapes and red wine, on ventricular remodeling after myocardial infarction (MI) in rats. After permanent ligation of the left anterior descending artery, surviving rats were randomly allocated to three groups and treated with 1 mg/kg/day resveratrol (R-1 group), 0.1 mg/kg/day resveratrol (R-0.

Caffeic acid phenethyl ester ameliorates cerebral infarction in rats subjected to focal cerebral ischemia.

The effects of caffeic acid phenethyl ester (CAPE), an antioxidant derived from propolis, on the infarct volume elicited by focal cerebral ischemia were studied on Long-Evans rats. Cerebral infarction was induced by microsurgical procedures with ligation of the right middle cerebral artery (MCA) and clipping of bilateral common carotid arteries (CCA) for 60 min. The rats were sacrificed 24 h later and serial brain slices of 2 mm thickness were taken and stained for the measurement of infarct area.

Antiarrhythmic effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia/reperfusion injury in rats.

Objectives: The present study was designed to determine the antiarrhythmic effect of caffeic acid phenethyl ester (CAPE), an active component of propolis, which exhibits antioxidant properties, in rats subjected to myocardial ischemia and ischemia-reperfusion (I/R) injury.

Design And Methods: Rats were subjected to 30 min coronary artery occlusion for evaluating the effect of CAPE on the myocardial ischemia injury. While in the myocardial I/R injury study, the coronary artery was ligated for a 5-min period of ischemia followed by a 30-min period of reperfusion.

The neuroprotective effect of glial cell line-derived neurotrophic factor in fibrin glue against chronic focal cerebral ischemia in conscious rats.

Glial cell line-derived neurotrophic factor (GDNF) is a transforming growth factor-beta which has shown beneficial effects in rats after acute focal cerebral ischemia (FCI). To study the effects of GDNF on chronic FCI injury in conscious rats, we used fibrin glue (GDNF-fibrin glue) and fibrin glue free (GDNF-only)-GDNF topically applied to the ischemic brain after right middle cerebral artery (MCA) ligation. Infarct brain volume and functional motor deficits were measured before and after FCI injury.

Effect of desflurane-induced preconditioning following ischemia-reperfusion on nitric oxide release in rabbits.

Nitric oxide (NO) is the mediator of ischemic preconditioning against myocardial infarction. Desflurane produces anesthetic preconditioning to protect the myocardium against infarction. In the model of myocardial ischemia-reperfusion injury in rabbits, we evaluated desflurane-induced ischemic preconditioning and studied its mechanism of NO synthesis.

The effect of desflurane on ameliorating cerebral infarction in rats subjected to focal cerebral ischemia-reperfusion injury.

To obtain more information on the cerebral ischemia and reperfusion injury under desflurane anesthesia, we compared the infarct volume and lactate dehydrogenase (LDH) activity in rats subjected to focal cerebral ischemia during different concentration of desflurane anesthesia. Male Long-Evans rats weighing 270-350 g were anesthetized with desflurane in air at 1.0, 1.

Preconditioned somatothermal stimulation on median nerve territory increases myocardial heat shock protein 70 and protects rat hearts against ischemia-reperfusion injury.

Objective: This study was designed to test the hypotheses that local somatothermal stimulation on the left median nerve territory increases myocardial heat shock protein 70 and that preconditioning of rats with local somatothermal stimulation protects the hearts against subsequent ischemia-reperfusion injury.

Methods: Local somatothermal stimulation was brought about by means of application of a heating rod over and above the left median nerve territory (1.5 cm proximal to the palm crease) in male Sprague-Dawley rats.

Honokiol ameliorates cerebral infarction from ischemia-reperfusion injury in rats.

Honokiol, a constituent extracted from Magnolia officinalis, had been shown be an antioxidant and an anti-platelet agent in biological systems with an anti-arrhythmic effect and a myocardial protective effect on ischemia-reperfusion injury. We examined the neuroprotective effect of honokiol in rats subjected to focal cerebral ischemia. Honokiol was administered intravenously either at fifteen minutes before right middle cerebral artery occlusion (pretreatment groups) or when both common carotid arteries clips were removed (treatment groups).