Administration of apocynin in drinking water ameliorates transient cerebral ischemia-induced brain damage and behavioral deficits in mice

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Administration of apocynin in drinking water ameliorates transient cerebral ischemia-induced brain damage and behavioral deficits in mice

Please use this identifier to cite or link to this item: http://hdl.handle.net/10355/15405

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Title: Administration of apocynin in drinking water ameliorates transient cerebral ischemia-induced brain damage and behavioral deficits in mice
Author: Lehmidi, Tareq Mohamed Elhadi
Keywords: ischemic stroke
oxidative stress
NADPH oxidase
superoxide radicals
Date: 2012
Publisher: University of Missouri--Columbia
Abstract: Acute ischemic stroke is the third leading cause of death in developed countries and the most frequent cause of permanent disability in adults worldwide. Despite advances in the understanding of the pathophysiology of cerebral ischemia, therapeutic options remain limited. Inflammation following ischemic stroke is known to contribute to neurological injury. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) is well known as a major source for superoxide radical generation in leukocytes. Superoxide radicals play a significant role in brain ischemia-reperfusion (I/R) injury. Recently, several forms of this oxidase have been found in a variety of non-immune cells including neurons and glial cells. Apocynin is a NOX inhibitor that has been studied as a potential treatment in experimental stroke. The anti-inflammatory activity of apocynin has been demonstrated in a variety of cells and animal models of inflammation. Apocynin after metabolic conversion, inhibits the assembly of NADPH oxidase that is responsible for reactive oxygen species (ROS) production. In our study, apocynin was used to test whether suppression of ROS by the NADPH oxidase inhibitor can protect against ischemia-induced ROS generation. Focal cerebral ischemia was induced in mice (C57BL/6J male mice) that used a dietary preventative protocol in which apocynin was added into the drinking water so that animals received 50mg/kg dose each day for 5 days before surgery (Intraluminal filament MCAO). Mice used were subjected to 90-120 minutes of focal ischemia induced by MCAO followed by 24 hrs reperfusion. Drinking apocynin group prior to ischemia significantly attenuated infarct volume and improved functional outcome. The neuroprotective effects of apocynin against ROS production during early phase I/R and subsequent I/R-induced neuronal damage provide strong evidence that inhibition of NADPH oxidase could be a promising therapeutic mechanism to protect against stroke damage in the brain.
URI: http://hdl.handle.net/10355/15405
Other Identifiers: LehmidiT-050412-T760
Rights: Access is limited to the University of Missouri - Columbia.

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