@article {44209,
	title = {Glibenclamide ameliorates ischemia-reperfusion injury via modulating oxidative stress and inflammatory mediators in the rat hippocampus.},
	journal = {Brain research},
	volume = {1385},
	year = {2011},
	note = {n/a},
	month = {2011 Apr 18},
	pages = {257-62},
	abstract = {<p>Stroke remains a debilitating disease with high incidence of morbidity and mortality, where many reports provide promising venues for prevention/treatment of such ailment. Glibenclamide, a selective blocker of KATP channels, was reported to protect against ischemia and ischemia-reperfusion (IR) injury in several experimental models. Hence, the present study aimed to investigate the possible involvement of free radicals as well as inflammatory and anti-inflammatory mediators in the hippocampus of rats exposed to IR. To this end, male Wistar rats were divided into 3 groups: group I served as sham operated controls; group II was subjected to 15 min ischemia by occlusion of both common carotid arteries, followed by 60 min reperfusion; group III was injected with glibenclamide (1mg/kg, i.p.) 10 min before ischemic-reperfusion injury. IR increased lipid peroxides, myeloperoxidase activity, TNF-α and PGE(2), while decreasing glutathione, total antioxidant capacity, nitric oxide and IL-10 levels in the hippocampus. Glibenclamide reversed all the former alterations, thus highlighting a potential therapeutic utility for this sulphonyl urea in IR brain injury via modulating oxidative stress and inflammatory mediators.</p>
},
	keywords = {Animals, Glyburide, Hippocampus, Inflammation Mediators, Male, oxidative stress, Random Allocation, Rats, Rats, Wistar, Reperfusion Injury},
	issn = {1872-6240},
	doi = {10.1016/j.brainres.2011.02.007},
	author = {Dalaal M. Abdallah and Noha N. Nassar and Rania M. Abd-El-Salam}
}
