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Oxidative stress,inflammation and apoptosis are involved in the pathological process after cerebral ischemic reperfusion injury.PicrodideⅡ could inhibit neuronal apoptosis and play ananti-oxidant role in cerebral ischemia/reperfusion injuries,but the exact mechanism needs to be further studied.In this study,a total of 90 adult,healthy,male Wistar rats were used to established the middle cerebral artery occlusion reperfusion (MCAO/R) models by intraluminal monofilament suture on the left external-internal carotid artery.The treatment groupand the positive control group were respectively injected with 1.0% picroside Ⅱ (10 mg/kg,250 μl) and salvianic acid A sodium (10mg/kg,250 μ l) via the tail vein,and the negative control group and sham-surgery group were injected with 0.1 mol/L phosphate buffer saline (PBS) 250 μ l.The results showed that that neurological behavioral malfunction appeared in all the rats with MCAO/R.The infarction focuses emerged in the ischemic hemisphere following the MCAO/R injuries.The number of apoptotic cells and the expression of inducible nitric oxide synthase (iNOS) increased while the superoxide dismutase (SOD) reduced after MCAO/R.After the treatment of picrodideⅡand salvianic acid A sodium,the nervous behavioral function improved,the infarction volume reduced,the number of apoptosis positive cells,the expressions and the concentrations in brain tissue of iNOS decreased while those of SOD increased significantly compared with the negative control groups (P<0.05).It is suggested that PicrodideⅡ might play a neuroprotective effect by inhibiting the neuronal apoptosisand the expressions of iNOS,and promoting the expression of SOD after cerebral ischemia/reperfusion injuries.