Role of c-jun N-terminal kinase cascade on neuronal protection with ischemic preconditioning in hippocampus in gerbil

Aim To investigate the role of c-jun N-terminal kinase cascade on neuronal protection with ischemic preconditioning in hippocampus in gerbil.Methods Forebrain ischemia was induced by occlusion of bilateral carotid arteries and confirmed by isoelectricity of EEG. Male gerbils were randomly divided into sham group(SH), ischemic-reperfusion group(IR), ischemic preconditioning group(IP), specific agonist of JNK-Anisomycin group(AN), specific antagonist of JNK-Curcumin group(CU), Anisomycin combined with IP(AP) group, Curcumin combined with IP(CP) group and solvent control group (VE). The gerbils were killed in 15min, 2, 4, 6 h, 1, 3, 5 and 7 d in each group following reperfusion. The number of apoptosis neurons in hippocampal CA1 region were counted. The activities of p-JNK and c-Jun expression in hippocampal CA1 region were detected using SP immunohistochemical technique. Results The number of apoptosis neurons were significant less and the levels of p-JNK or Jun expression were markedly decreased in hippocampal CA1 region in each point in group IP, CU and CP than that in group IR(P0.01). This effect was less in group IP than in group CP, but was more than in group CU. Anisomycin could increase the number of apoptosis neurons(vs IR,P0.01) and the levels of p-JNK expression at 15 min, 2, 4, 6 h or Jun expression at 1, 3, 5 and 7 d(vs IR,P0.01) after reperfusion. Anisomycin combined with IP could partly counteract neuroprotective effects of IP. Conclusion Activation of JNK cascade in hippocampal CA1 region may participate in neuroal ischemic injury and apoptosis. Ischemic preconditioning display neuroprotective effects by inhibiting the expression of JNK and Jun in hippocampal CA1 region. Inhibition JNK cascade may educe the resemble neuroprotective effects of IP.