Dr. Rania Mohsen AbdElSalam

Citation:

Abdallah, D. M., N. N. Nassar, and R. M. Abd-El-Salam, "Glibenclamide ameliorates ischemia-reperfusion injury via modulating oxidative stress and inflammatory mediators in the rat hippocampus.", Brain research, vol. 1385, pp. 257-62, 2011 Apr 18.

Abstract:

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.

Notes:

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