To study the protective effect of rosuvastatin on ischemic brain injury and its mechanism,in on ischemic brain injury and its mechanism,focal cerebral ischemia/reperfusion was induced by occlusion of the middle cerebral artery (MCA)-luminal filament technique. The cerebral blood flow was monitored with laser-Doppler flowmetry (LDF). The slices of brain tissue were stained with cresyl-violet. The cerebral e quantified with ImageJ software. The expressions of endothelial NO synthase (eNOS) and activated caspase-3 were detected with Western blot. The inducible NO were immunohistochemically observed. The results demonstrated that rosuvastatin (20 mg/kg) could remarkably decrease infarct volume and cerebral edema after MCAO ots showed that the expression of eNOS in cerebral cortex before and after ischemia was (100±43.3) %, (1668.9±112.2) % respectively (P＜0.001), rosuvastatin gulated the expression of eNOS in non-ischemic cortex (P＜0.001), whereas in ischemic cortex of rosuvastatin group the expression of eNOS was (1678.8±121.3) %. There was no hemic cortex, nonetheless the expression of activated caspase-3 increased after ischemia, and rosuvastatin significantly diminished it (P＜0.01). Immunoaled no iNOS-positive cells in non-ischemic brain area, while in ischemic brain area the number of iNOS positive cells went up, and rosuvastatin could significantly reduced them.'s neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3.mia/reperfusion; NOS; caspase-3