低氧预适应升高小鼠脑内JNK磷酸化水平和蛋白表达  

Hypoxic preconditioning increases JNK phosphorylation and protein expression levels in brain of mice

作　　者：高歌[1] 龙彩瑕[1] 高亚南[1] 牛晨晨[1] 徐群渊[1] 李俊发[1] 

机构地区：[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,北京100054

出　　处：《基础医学与临床》2006年第2期139-142,共4页Basic and Clinical Medicine

基　　金：国家自然科学基金(30270508;30470650);北京市自然科学基金(7032005);教育部优秀青年教师资助项目;北京市教委科技发展计划项目(KM200310025100)

摘　　要：目的探讨C-JUN氨基末端激酶或应激激活蛋白激酶（JNKs／SAPKs）在脑低氧预适应发生、发展过程中的作用。方法将小鼠整体低氧预适应模型中BALB／C小鼠随机分为正常对照（H0）、早期（H1-H4组）和延迟性（H5-H6组）低氧预适应等7组。应用SDS-PAGE和Western bolt方法，并结合GelDoc凝胶成像系统，半定量检测大脑皮层和海马组织内JNK1和JNK2／3的磷酸化水平及其蛋白表达量的变化。结果在早期低氧预适应形成过程中，随低氧次数的增加，小鼠大脑皮层和海马组织内JNK1的磷酸化水平（未检测到磷酸化的JNK2／3）逐渐升高，且以皮层内（H1和H2组）和海马组织内（H1—H4组）的增高明显（P〈0．05，n=6）；而JNK1和JNK2／3只在延迟性低氧预适应（H5-H6组）发展过程中明显上调（P〈0．05，n=6）。结论JNK1的激活以及JNK1和JNK2／3蛋白表达量的增高可能分别参与了脑早期低氧预适应和晚期延迟性低氧预适应的发生和发展。Objective To explore the role of C-JUN N-terminal kinases/stress activated protein kinases （JNKs/SAPKs） in the development of cerebral hypoxic preconditioning. Methods Healthy adult BALB/C mice weighing 18 - 20 g regardless of sex were randomly divided into 7 groups（at least n = 6 for each group）： control （H0）, early hypoxic preconditioned （H1 - H4, repetitive hypoxic exposure for 1 -4 times respectively） and delayed hypoxic preconditioned （H5 and H6, some mice of group H4 were kept in the normoxic condition for 24 hours for recovery before the fifth and sixth hypoxic insult on the following day） groups. SDS-PAGE, Western blot and Gel Doe imagine systems were applied to semiquantitatively analyze the levels of JNKs phosphorylation and protein expression in brain of hypoxic preconditioned mice. Results We found that the phosphorylation levels of JNK1 not JNK2/3 were increased significantly （ P 〈 0.05） both in cortex（H1-H2）and hippocampus （H1-H4）, while no significant changes in JNK1 and JNK2/3 protein expression were found both in cortex and hippocampus of early hypoxic preconditioned mice. In addition, the protein expression levels of JNK1 and JNK2/3 were also increased significantly （ P 〈 0.05） both in cortex and hippocampus of delayed hypoxic preconditioned mice （H5-H6）. Conclusion Results suggested that the activation of JNK1, and increment of JNK1 and JNK2/3 protein expression might be involved in the development of early and delayed hypoxic preconditioning respectively.

关 键 词：脑低氧预适应 JNK 磷酸化 蛋白表达量 脑组织 

分 类 号：R741[医药卫生—神经病学与精神病学]