Neuroprotection By S-Pbn In Hyperglycemic Ischemic Brain Injury

Background: Hyperglycemia exacerbates focal ischemic brain damage supposedly through various mechanisms. One such mechanism is oxidative stress involving reactive oxygen and nitrogen species (RONS) production. Nitrones attenuate oxidative stress in various models of brain injury. Sulphonated nitrones are hydrophilic and highly feasible to administer in experimental settings. Sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) has been shown neuroprotective in experimental brain trauma. Together with the theories on increased oxidative stress in focal brain ischemia with concomitant hyperglycemia, we hypothesised that S-PBN might be neuroprotective under those circumstances as well. Material and methods: The rats were made hyperglycemic by intraperitoneal bolus of glucose (2 g/kg) and then subjected to 90 min transient middle cerebral artery occlusion (MCAO). They were randomised to a therapeutic regime of S-PBN (47 mg/kg) or saline given intravenously. Neurological testing and tetrazolium red staining were performed after 1 day. Results: S-PBN improved the neurological performance at day 1 both in Bederson score (1,3 +/- 0,8 vs. 2,7 +/- 0,48)(figure 1) and on the inclined plane [74,5% +/- 4,6 (S-PBN) vs. 66% +/- 8,3 (control) P< 0.05] (figure 2); but did not reduce the infarct size (figure 3). Physiological data did not differ between groups (table1).