Objective To investigate the role of JNK in IP induced tolerance against forebrain ischemia reperfusion injury in gerbils. Methods Two hundred and eighty-eight gerbils weighing 50 g^70 g were randomly divided into six groups. Gerbils were anesthetized with intraabdominal pentobarbital sodium 40 mg/kg. Forebrain ischemia was induced by occlusion of bilateral carotid arteries. In sham group, bilateral carotid arteries were dissected and isolated but not occluded. In IC (ischemic preconditioning control) and IR (ischemia/reperfusion) group, bilateral carotid arteries were dissected and isolated and temporarily clamped for 3 min and 5 min respectively and then released for reperfusion. In IP (ischemic preconditioning) group, 5 min of cerebral ischemia were performed 3 d after 3 min of cerebral ischemia. In CU group curcumin 20 mg/kg intraperitoneally injected 1 h before 5 min of cerebral ischemia. Same volume of DMSO intraperitoneally injected 1 h before 5 min of cerebral ischemia as DMSO group. The gerbils were sacrificed at 15 min, 2 h, 4 h, 6 h, 1 d, 3 d, 5 d and 7 d in each group following reperfusion. Open field test was used to examine the behavioral deficit in the due time. The number of surviving and apoptosis neurons in hippocampal CA1 region was counted, and the activity of p-JNK and p-c-Jun in CA1 region was detected by SP immunocytochemical technique. Results The behavioral mark and the number of apoptosis neurons in hippocampal CA1 region in group IP were much less than that in IR group (P﹤0.01). The p-JNK in IR group were markedly expressed in CA1 region, especially at 1 d after reperfusion. The levels of p-JNK in CA1 region were much lower in group IP than that in group IR (P﹤0.01). p-c-Jun also markedly expressed in CA1 region and reached the peak expression at 6 h after reperfusion in IR group. Curcumin remarkably suppressed the expression of p-JNK and p-c-Jun in CA1 region, and can mimic the effect of IP. Conclusion Cerebral ischemia could cause p-JNK to be expressed markedly in gerbil hippocamp
