BACKGROUND Although agmatine therapy in a mouse model of transient focal cerebral ischemia is highly protective against neurological injury, the mechanisms underlying the protective effects of agmatine are not fully elucidated. This study aimed to investigate the effects of agmatine on brain apoptosis, astrogliosis and edema in the rats with transient cerebral ischemia. METHODS Following surg...

Hypoxia is a critical factor for cell death or survival in ischemic stroke, but the pathological consequences of combined ischemia-hypoxia are not fully understood. Here we examine this issue using a modified Levine/Vannucci procedure in adult mice that consists of unilateral common carotid artery occlusion and hypoxia with tightly regulated body temperature. At the cellular level, ischemia-hyp...

BACKGROUND AND PURPOSE Neuroinflammation plays a critical role in the pathogenesis of cerebral ischemia. Triflusal, a selective cyclooxygenase-2, and its active metabolite 3-hydroxy-4-trifluoromethylbenzoic acid may inhibit apoptosis and inflammation after cerebral ischemia. An in vivo model of cerebral ischemia was used to investigate the effects of triflusal and aspirin treatment on infarct v...

PURPOSE Cerebral ischemia/reperfusion (I/R) injury causes hippocampal apoptosis and cognitive impairment, and the dysfunction of gap junction intercellular communication (GJIC) may contribute to the cognitive impairment. We aim to examine the impact of cerebral I/R injury on cognitive impairment, the role of GJIC dysfunction in the rat hippocampus and the involvement of the phosphatidylinositol...

Our recent findings indicate an induced upregulation of 14-3-3c mRNA and protein in ischemic cortical astrocytes. Despite being brain-specific, the functional role of 14-3-3c in the brain still remains largely unknown. In this study, we show that among all the 14-3-3 isoforms, only the c isoform is inducible under ischemia in astrocytes. Furthermore, this upregulation of 14-3-3c may play a spec...

Background: Nitric oxide synthase (NOS) activity is increased during hypertension and cerebral ischemia. NOS inactivation reduces stroke-induced cerebral injuries, but little is known about its role in blood-brain barrier (BBB) disruption and cerebral edema formation during stroke in acute hypertension. Here, we investigated the role of NOS inhibition in progression of edema formation and BBB d...

Naloxone was given as an I.V. bolus of 0.8 mgs to four groups of patients with stroke: 1) 20 patients with C.T. proven cerebral infarcts of longer than 7 days duration; 2) 20 patients with acute cerebral ischemia of less than 24 hours; 3) 5 patients with C.T. proven intracerebral hemorrhage of less than 24 hours, and; 4) 3 patients with hyperacute cerebral ischemia which occurred during the per...

BACKGROUND AND PURPOSE Vascular endothelial growth factor (VEGF) is a major mediator of angiogenesis and a strong vascular permeability factor. VEGF is known to open the blood-brain barrier (BBB) and induce cerebral edema. Experimental studies of VEGF antagonism have shown it reduces cerebral edema after ischemia, indicating its potential for prevention of secondary brain damage. We examined th...

Background: The role of nitric oxide (NO) of endothelial or neuronal origins in cerebral ischemia and reperfusion injuries are far from being settled, extending from being important to not having any role at all.  Objective: To investigate the role of NO of endothelial and neuronal origins in ischemia/reperfusion injuries in focal cerebral ischemia, L-NAME, a non selective NO synthase inhibitor...

background: the role of nitric oxide (no) of endothelial or neuronal origins in cerebral ischemia and reperfusion injuries are far from being settled, extending from being important to not having any role at all.    objective: to investigate the role of no of endothelial and neuronal origins in ischemia/reperfusion injuries in focal cerebral ischemia, l-name, a non selective no synthase inhibit...