Abstract
Cerebral ischemic reperfusion injury is a heterogeneous phenomenon with a multi-factorial etiology, and characterized as a cascade of neurochemical processes evolving in time and space after restriction or sudden interruption of cerebral blood flow. It has been suggested that oxidative stress and nitrosative stress are important mechanisms in cerebral ischemic reperfusion. The concept of oxidative and nitrosative stress stem from the generation of the reactive oxygen species (ROS) involving the nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) family and the reactive nitrogen species (RNS) including nitric oxide (NO) and peroxynitrite (ONOO−) at rates which exceed the capacity of natural antioxidant and anti-nitrification defense mechanisms to detoxify these toxic products. This review is focusing on the role of oxidative and nitrosavtive stress in cerebral ischemic reperfusion injury by discussing the concepts, the mechanisms, and the pharmacological approaches of ROS and RNS modulation for preventing cerebral ischemic reperfusion injury.
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