Figure 1.

Acute neuroprotection by corticosteroids requires eNOS. (a) Dose–dependent effects of dexamethasone (Dex) on stroke volume derived from TTC-stained (24 hours) or hematoxylin and eosin–stained (72 hours) brain sections after MCAo (n = 8–11). *P < 0.05 vs. vehicle. (b) Effects of delayed steroid treatment on neuroprotection. Shown is a schema of treatment regimens and corresponding cerebral infarct reduction by dexamethasone relative to the vehicle (Veh) group (n = 7–11). *P < 0.05 vs. vehicle. (c) Infarct volume corrected for edema in wild-type and eNOS^–/– mice treated with vehicle or dexamethasone (20 mg/kg bolus administered intraperitoneally [i.p.]) 24 hours after MCAo (n = 5–11). Wild-type mice are identical to those in (a). *P < 0.05 vs. all other groups; WT, wild-type. (d) The eNOS protein and mRNA levels after steroid treatment. Equal amounts of aortic tissue homogenates (40 μg) were immunoblotted against eNOS followed by stripping and reprobing against actin (top panels). A representative experiment is shown. Three separate experiments yielded similar results. Brain eNOS mRNA expression from mice treated with vehicle or dexamethasone with or without RU486 (RU) or LY294002 (LY) for 24 hours is shown in the lower panel. The corrected eNOS mRNA levels (eNOS/GAPDH) were determined by real time PCR (n ≥ 3 for each condition). t, time.