OBJECTIVE The purpose of this study was to obseve the protective effects of OSR(oxysophoridine,OSR) on cerebral ischemia and reperfusion injury in mice and to explore its possible protective mechanism.METHODS ICR mice were divided into a sham-operated group,a vehicle group,OSR(62.5,125,250 mg·kg-1) groups and a nimodipine(6 mg·kg-1) group.I.p.administration of OSR(62.5,125,250 mg·kg-1) in OSR groups for 7 d,ig administration of nimodipine(6 mg·kg-1) in nimodipine group for 7 d,ip administration of the same volume saline in sham-operated group and vehicle group for 7 d.Mice models of focal cerebral ischemia and reperfusion injury were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion except the sham-operated group.After 24 h of reperfusion,mice were tested for neurological deficit scores with the method of Bederson′s score,the cerebral infarct volume were assessed with the method of TTC staining in mice,the brain water content were determined by dry/wet weight method and the cerebral index were counted in mice,the levels of adenosine-triphosphate(ATP),maleic dialdehydle(MDA),glutathione peroxidase(GSH-PX),superoxide dismutase(SOD),catalase(CAT),nitric oxide(NO),nitric oxide synthase(NOS) and lactate dehydrogenase(LDH) in the brain tissues were measured with the method of spectrophotometry.RESULTS Compare to the model group,OSR(125,250 mg·kg-1) and nimodipine(6 mg·kg-1)reduced the neurological deficits scores(P<0.01) and the cerebral infarct volume(P<0.05).Compare to the model group,OSR(62.5,125,250 mg·kg-1) and nimodipine(6 mg·kg-1)reduced the brain water content(P<0.01).Compare to the model group,OSR(125,250 mgp·kg-1) and nimodipine(6 mg·kg-1)reduced the cerebral index(P<0.05).Compare to the model group,OSR(62.5,125,250 mg·kg-1) and nimodipine(6 mg·kg-1)reduced the contents of MDA,NO(P<0.01) and increased the contents of ATP(P<0.01).Compare to the model group,OSR(62.5,125,250 mg·kg-1) and nimodipine(6 mg·kg-1)enhanced the activities of SOD,GSH-PX,LDH and CAT(P<0.01),also decreased the activity of NOS(P<0.01).CONCLUSION OSR has significant protective effects of cerebral ischemia and reperfusion injury in mice,the effective mechanism of OSR might relate to the alleviation of oxidative stress. OBJECTIVE The purpose of this study was to obseve the protective effects of OSR (oxysophoridine, OSR) on cerebral ischemia and reperfusion injury in mice and to explore its possible protective mechanism. METHODS ICR mice were divided into a sham-operated group, a vehicle group , OSR (62.5,125,250 mg · kg -1) groups and a nimodipine (6 mg · kg -1) group.Ipadministration of OSR (62.5,125,250 mg · kg -1) in OSR groups for 7 d, ig administration of nimodipine (6 mg · kg -1) in nimodipine group for 7 d, ip administration of the same volume of saline in sham-operated group and vehicle group for 7 d .Mice models of focal cerebral ischemia and reperfusion injury were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion except the sham-operated group. After 24 h of reperfusion, mice were tested for neurological deficit scores with the method of Bederson’s score, the cerebral infarct volume were assessed with the method of TTC staining in mice, the brain water content were d etermined by dry / wet weight method and the cerebral index were counted in mice, the levels of adenosine-triphosphate (ATP), maleic dialdehyde (MDA), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD) , nitric oxide (NO), nitric oxide synthase (NOS) and lactate dehydrogenase (LDH) in the brain tissues were measured with the method of spectrophotometry .RESULTS Compare to the model group, OSR (125,250 mg · kg -1) and nimodipine Compare to the model group, OSR (62.5,125,250 mg · kg -1) and nimodipine (6 mg · kg -1) reduced the neurological deficits scores (P <0.01) and the cerebral infarct volume (P <0.01) .Comparison of the model group, OSR (125,250 mgp · kg-1) and nimodipine (6 mg · kg- (P <0.01) and increased the contents of ATP (P <0.01). Compare to the model group, OSR (62.5,125,250 mg · kg -1) and nimodipine (6 mg · kg -1) Compare to the model group, OSR (62.5, 125, 250 mg · kg -1) and nimodipine (6 mg · Kg-1) enhancedthe activities of SOD, GSH-PX, LDH and CAT (P <0.01), also decreased the activity of NOS (P <0.01) .CONCLUSION OSR has significant protective effects of cerebral ischemia and reperfusion injury in mice, the effective mechanism of OSR might relate to the alleviation of oxidative stress.