Objective:To study the effect of the inhibitor of p38MAPK(SB202190)on focal cerebral ischemia/reperfusion in rats,and furth explore the nourprotective effect and mechanism of SB202190 on focal cerebral ischemia/reperfusion. Methods: The acute focal cerebral ischemia/reperfusion models were established by suture emboli. Healthy male Sprague-Dawley rats were randomly divided into five groups:normal control group,sham group,ischemia/reperfusion group,SB202190 and DMSO group. In SB202190 and DMSO group,SB202190(the specific inhibitor of p38MAPK) and 1 % dimetyl sulphoxide(DMSO) were injected into the lateral ventricle respectively. Behavior scores of rat neuralogical fanction were penformed for each group The rats were sacrificed at 24 h after ischemia/reperfusion. Nissl staining is rsed to observe morphologic changes of neuron cells in ischemia/reperfusion injury region;and immunohisochemistry is used to detect Bcl-2 and Bax protein positive cell. Results: Rats of ischemia/reperfusion group had a lower score of neurological function compared with sham group(P < 0.05). The score in SB202190 group was significantly higher than that in ischemia/reperfusion group(P < 0.05),but there was no difference between ischemia/reperfusion group and DMSO group(P > 0.05).There were massive cellular necrosis found in rats at 24 h after ischemia/reperfusion,the form of neuron cell were atrophica,cellular plasm dried up and nucleus were densely stained,intercellular space were more lager than normal neuron cell. SB202190 group:Compared with the ischemia/reperfusion group,the cellular swelling was more light at 24 h after ischemia/reperfusion,and the injury of cellular necrosis was mild after ischemia/reperfusion;Immunohisochemistry staining to detect Bcl-2 and Bax positive neurons:There were a few Bcl-2 and Bax positive cells,which distributed dispersively in ischemia/reperfusion injury region,and there was no obvious difference between normal control group and sham group(P > 0.05);For the Ischemia/reperfusion group:There were massive Bax positive cells distributed in ischemia/reperfusion injury region at 24 h after ischemia/reperfusion,but Bcl-2 positive cells were no obvious change(P > 0.05);For the SB202190 group:Bcl-2 positive cells obvious increased at 24 h after ischemia/reperfusion(P > 0.05),but Bax positive cells obvious decreased compared with the Ischemia/reperfusion group. Conclusion:The inhibitor of p38MAPK(SB202190) can protect neural function from ischemia/reperfusion injury after ischemia/reperfusion in rat. SB202190 can reduce the region of ischemia/reperfusion injury,and regulate the activation of Bcl-2 and Bax protein after ischemia/reperfusion in rat,and it may be one of the possible mechanisms of antiapoptotic effect of SB202190.