Neuroprotective potential of glibenclamide is mediated by antioxidant and anti-apoptotic pathways in intracerebral hemorrhage.

The sulfonylurea receptor 1 (SUR1)-regulated NCca-ATP channels were progressively upregulated and demonstrated unchecked opening in central nervous system (CNS) injury, which induced cerebral damage. Glibenclamide (GLI) can block NCca-ATP channels and consequently exert protective effects. Recent studies have found that GLI has antioxidative effects. In this study, we primarily explored the antioxidative effects of GLI in a rat model of intracerebral hemorrhage (ICH). We found that GLI could scavenge free radicals, reduce activated-caspase-3 expression, increase the Bcl-2/Bax ratio, inhibit apoptosis, and improve functional neurological outcomes in a rat model of ICH.