Abstract: Objective To explore initially the role of c-Jun N-terminal protein kinases (JNK) in cerebral ischemia preconditioning.Methods Healthy adult SD rats were randomly divided into 5 groups: control group, sham-operated group, ischemic preconditioning or ischemic tolerance group, bee venom group, peripheral noxious tolerance group. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to determine the JNK phosphorylation and protein expression in somatosensory cortex and hippocampus. Results The phosphorylation level of JNK46KD but not JNK54KD in somatosensory cortex increased significantly (P<0.05) after ischemia preconditioning, while no significant changes had been observed in that of JNK46KD and JNK54KD in hippocampus. In addition, the protein expression level of JNK46KD but not JNK54KD fell on control level in somatosensory cortex after ischemic preconditioning, while no significant changes in JNK46KD and JNK54KD protein expression were found in hippocampus. Conclusion The increased JNK46KD phosphorylation and fallen JNK46KD protein expression in somatosensory cortex may be involved in the development of cerebral ischemia preconditioning.

Key words: cerebral ischemic preconditioning, c-Jun N-terminal protein kinases (JNK), phosphorylation, protein expression