Glucocorticoid Receptor Blockers Pretreatment Did Not Improve Infarct Volume in Type-2 Diabetic Mouse Model of Stroke

Impaired glucocorticoid signaling in diabetes mellitus and its relation to suppressed immune function hyperglycemia during acute stroke has been shown be detrimental. Therefore, the aim of this study was examine effect receptor (GCR) blockers a type-2 diabetic mouse model following hypoxia–ischemia (HI). We induced db/db non-diabetic db/+ mice by unilateral common carotid artery ligation followed 20 min HI. Mice were pretreated with RU-486, GCRII blocker (40 mg/kg), intraperitoneally, day before, post-HI. Blood brain samples collected at 24 h post-HI measure blood glucose, corticosterone infarct size. Similarly, another set RU-486 + spironolactone, GCR1 (25 mg/kg) subcutaneously for week before inducing recovery. Samples 48 various analyses. treatment did not lower glucose significantly, but spironolactone decreased However, none groups ischemia-induced serum level or This suggests that even though GCR improve hyperglycemia, they volume.