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dc.contributor.advisorGu, Zezongeng
dc.contributor.authorLehmidi, Tareq Mohamed Elhadieng
dc.date.issued2012eng
dc.date.submitted2012 Springeng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on September 19, 2012).eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionThesis advisor: Dr. Zezong Gueng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionM.S. University of Missouri-Columbia 2012.eng
dc.description"May 2012"eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] 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.eng
dc.format.extentxiii, 71 pageseng
dc.identifier.merlinb94297988eng
dc.identifier.oclc818865324eng
dc.identifier.urihttps://hdl.handle.net/10355/15405
dc.identifier.urihttps://doi.org/10.32469/10355/15405eng
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess to files is limited to the University of Missouri--Columbia.eng
dc.subjectischemic strokeeng
dc.subjectoxidative stresseng
dc.subjectNADPH oxidaseeng
dc.subjectsuperoxide radicalseng
dc.subject.meshIschemic Attack, Transient -- drug therapyeng
dc.subject.meshNADPH Oxidase -- metabolismeng
dc.subject.meshReperfusion Injury -- drug therapyeng
dc.subject.meshReactive Oxygen Species -- agonists & inhibitorseng
dc.subject.meshOxidative Stress -- drug effectseng
dc.subject.meshAcetophenones -- pharmacologyeng
dc.subject.meshAcetophenones -- therapeutic useeng
dc.titleAdministration of apocynin in drinking water ameliorates transient cerebral ischemia-induced brain damage and behavioral deficits in miceeng
dc.typeThesiseng
thesis.degree.disciplinePathology (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.S.eng


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