【Abstract】Objective To Apoptosis effect of SP600125 on cerebral ischemia/reperfusion in rats and its possible mechanism. Methods 54 SD rats weighing 230 g-250 g were randomly divided into sham operation group(SH), ischemia/reperfusion group(IR) or JNK inhibitor SP600125 group(SP). The rats were given dimethyl sulfoxide(DMSO, SH group), DMSO(I/R group ) or SP600125(SP group, the use of DMSO solvent) of 30 min before ischemia respectively by intracerebroventricular injection. Each group divided into 3 subgroups according to reperfusion time 30 min, 24 h and 72 h(each subgroup of 6 animals). The establishment of SD rat model of global cerebral ischemia was induced by four-vessel occlusion, in cerebral ischemia-reperfusion after 24, 72 h to determine his behavior. The number of survival pyramidal cells bax and bcl-2 positive pyramidal cells in the CA1 subfield of hippocampus were counted at the time points of 30 min, 24 h and 72h after reperfusion were immunohistochemical methods and TUNEL. Results As compared with vehicle treatment, penehyclidine hydrochloride treatment increased the standing times （4.8±2.0, 9.1±3.4）(P<0.05), and the beam-walking test scores（2.3±1.2, 3.5±0.9）（P<0.05）. Immunohistochemistry results showed that after I/R Hippocampal CA1 area Bcl-2 and Bax positive expression increased the number of pyramidal cells, 24 h of reperfusion the number of pyramidal cells shows that the expression of positive to the peak（40.5±5.1）(P<0.01),After ischemia-reperfusion 24 h to 72 h, Positive expression to reduce the number of pyramidal cells(P<0.05)，With the I/R group, SP group Bcl-2-positive pyramidal cells increased the number of（89.7±8.4）(P<0.05),Bax-positive increase in the number of pyramidal cells less（40.5±2.3）(P<0.05). Conclusion SP600125 protects the neurons from apoptosis and death in rat hippocampal CA1 region during whole brain ischemia/reperfusion injury.This mechanism involves the inhibition of JNKsignal transduction pathway.