Abstract: ［Abstract］ Objective〖HTSS〗〓To investigate the role of p38 MAPK signaling pathway in sulbactaminduced brain ischemic tolerance in rats.
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓The model of rat global cerebral ischemia was used. After a stainless steel cannula was implanted in the right lateral ventricle，25 healthy male Wistar rats were randomly divided into the following groups(n=5 in each group). ①Sham group（normal saline+sham）: the rats were administrated with normal saline of 10 μL via the cannula first, and then the sham operation for global cerebral ischemia was performed. ②Global cerebral ischemia group（ischemia）: normal saline(10 μL) was administrated via the cannula first and then performed 8 minutes of global cerebral ischemia immediately. ③Sulbactam+ischemic group: sulbactam solution(10 μL, 360 nmol) was administrated via the cannula first and then performed 8 minutes of global cerebral ischemia immediately. ④SB203580+sulbactam+ischemic group: SB203580(10 μL, 5 nmol) was administrated via the cannula 30 minutes before sulbactam(10 μL, 360 nmol) and then performed 8 minutes of global cerebral ischemia immediately. ⑤SB203580+sham group: SB203580 solution(10 μL, 5 nmol) was administrated via the cannula first and then performed sham operation for global cerebral ischemia immediately. The neuropathological evaluation including histological grade(HG) and neuronal density(ND) was performed using the method of thionic staining to observe the survival situation of neurons in CA1 hippocampus.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓Global cerebral ischemia for 8 min induced obvious delayed neuronal death（DND）which resulted in large area of neuronal absence in the CA1 hippocampus with the significant increase in HG and decrease in ND. Pretreatment with sulbactam effectively prevented the DND normally induced by the global brain ischemia. Compared with ischemic group，the HG was significantly reduced, and the ND increased significantly. Pretreatment with SB203580, an inhibitor of p38 MAPK signal pathway, blocked the neuroprotective effect mediated by sulbactam. Compared with sulbactam+ischemic group, the ND was significantly decreased, and the HG increased significantly.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓p38 MAPK signaling pathway may participate in the sulbactaminduced brain ischemic tolerance in rats.

Key words: hypoxia, brain, sulbactam, rat