脑缺血预适应大鼠脑内c-Jun氨基末端激酶磷酸化水平和蛋白表达量的改变

Phosphorylation and Protein Expression of c-Jun N-Terminal Protein Kinases in Cerebral Ischemia Preconditioning Rats

目的初步探讨c-Jun氨基末端激酶(JNK)在大鼠脑缺血预适应中(IPC)的作用。方法将大鼠随机分为正常对照(control)、假手术(SI)、缺血预适应或缺血耐受(IT)、单纯蜜蜂毒(BV)、外周伤害耐受(PNT)5组。应用SDS-PAGE、Western blot等实验方法,借助GelDoc和Versa Doc凝胶成像系统,半定量检测大脑躯体感觉皮层、海马组织内JNK的磷酸化水平和蛋白表达量的变化。结果IPC大鼠大脑躯体感觉皮层内JNK46KD的磷酸化水平(激活程度)增高(P<0.05),JNK54KD及海马组织内JNK46KD和JNK54KD的磷酸化水平无明显变化。IPC大鼠躯体感觉皮层JNK46KD蛋白表达量回落(P<0.05),JNK54KD及海马组织内JNK46KD和JNK54KD的蛋白表达量均无明显变化。结论大鼠躯体感觉皮层内JNK46kDa磷酸化水平的增高及其蛋白表达量的回落可能参与了脑缺血预适应的形成。

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 precondi tioning 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 hippocam pus. 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 de- velopment of cerebral ischemia preconditioning.