Objective To compare the expression of Ku70 and Bax in hippocampus CA1 between normal rats and diabetic rats following cerebral ischemia/reperfusion,so as to explore the roles of Ku70 and Bax in aggravating cerebral ischemia/reperfusion injury in diabetes. Methods Totally 72 male SD rats were divided into 3 groups randomly: sham operated (SO) group, normoglycemia global cerebral ischemia/reperfusion (NCI) group, and diabetic global cerebral ischemia/reperfusion (DCI) group. The rats in DCI group were treated by streptozocin (STZ) and improved Pulsinelli’s four-vessel occlusion method to establish diabetic global cerebral ischemia/reperfusion model. And animals in NCI group were not given STZ, and other treatments were similar to those in the DCI group. Animals in the SO group only had blood vessels exposed. Changes of neuron pathology in hippocampus CA1 were observed by H-E staining under light microscopy at 1, 6, 24, and 48 h after ischemia/reperfusion; expression of Ku70 was detected by immunohistochemistry and Western blotting analysis, and expression of Bax was detected by immunohistochemistry. Results The neuron structure in hippocampus CA1 of rats was damaged in NCI group, and the density of survival neurons was significantly lower than that in the SO group at all studied time points(P<0.05); the neuron structure damage in DCI group was more severe, and the density of survival neurons was significantly lower than that of the NCI group at all studied time points(P<0.05). The expression of Ku70 at 1 and 6 h in NCI group was significantly higher than that in the SO group (P<0.05), and that at 24 and 48 h was significantly lower than that in the SO group(P<0.05); Ku70 expression in DCI group was significantly lower than that in the NCI group at all studied time points(P<0.05). Bax expression in NCI group was significantly higher than that in the SO group at all studied time points(P<0.05), and that in DCI group was significantly higher than that in the NCI group at all studied time points (P<0.05). Conclusion Diabetes can aggravate global cerebral ischemia/reperfusion injury, which may be related to aggravated Ku70 expression decrease and Bax expression increase.