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Introduction
Brain edema is an abnormal accumulation of fluid in the brain parenchyma, and is a dangerous complication of stroke as it worsens the primary ischemic injury of the brain [1]. Prevention of brain edema formation may reduce mortality rates in ischemic stroke. Ischemic brain edema happens in 2 phases: cytotoxic edema, which develops within the first minutes to hours following ischemia, and vasogenic edema, which is permanent and takes hours to days to occur [2]. Vasogenic edema is characterized by an enlarged extracellular volume due to damage to the brain capillaries and leakage of plasma proteins such as albumin [3]. Vasogenic edema increases the risk for hemorrhage from impaired vessels [4] and cerebral herniation [2].
Oxidative stress has been shown to be involved in ischemia/reperfusion neuronal injury [5]. Reactive oxygen species (ROS) generated during cerebral ischemia and reduction of the brain antioxidant capacity are the most important causes of ischemic neuronal damage [6]. Incremental ROS production causes damage to lipid membranes and nucleic acids, and may lead to cell death. Generation of the ROS is further increased by reperfusion because an abrupt return of glucose and oxygen to the neurons causes free radical production at higher levels [7]. Strategies based on antioxidant supplementation have been shown to produce protective effects against brain injury in experimental models [8]. α-Tocopherol, as a potent antioxidant, is the most important form of vitamin E. It has been reported that exogenous administration of α-tocopherol produces neuroprotective effects against cerebral ischemic injury, most probably by a reduction of ROS formation and the inhibition of inflammation and apoptosis [9,10]. However, there are no data about the effects of α-tocopherol on vasogenic brain edema formation and blood-brain barrier (BBB) disruption following ischemia. Therefore, this study was conducted to investigate the effects of α-tocopherol supplementation on ischemic brain edema formation, BBB permeability and oxidative stress biomarkers in the rat brain following transient focal cerebral ischemia.
Materials and Methods
Animals
Ninety-six male normotensive Sprague Dawley rats (280-320 g) were obtained from the central animal house facility of Ardabil Medical Sciences University, Ardabil, Iran. All protocols of the study were approved by the Institutional Animal Ethics Committee of Ardabil Medical Sciences University, which follows the NIH guidelines for the care and use of animals. The...