《中国康复理论与实践》

《中国康复理论与实践》 ›› 2007, Vol. 13 ›› Issue (07): 623-625.

• 基础研究 • 上一篇    下一篇

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

赵兰峰; 郭社卫; 安仰原; 刘明刚   

  1. 首都医科大学神经生物学系,疼痛生物医学研究所,北京神经再生修复重点实验室,北京市 100069
  • 收稿日期:2007-04-03 出版日期:2007-07-01 发布日期:2007-07-01

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

ZHAO Lan-feng, GUO She-wei, AN Yang-yuan, et al   

  1. Institute for Biomedical Sciences of Pain, Beijing Key Laboratory for Neural Regeneration and Repairing, Department of Neurobiology, Capital Medical University, Beijing 100069
  • Received:2007-04-03 Published:2007-07-01 Online:2007-07-01

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摘要： 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。

关键词: 脑缺血预适应, c-Jun氨基末端激酶(JNK), 磷酸化, 蛋白表达

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