中文摘要：

目的：初步探讨丝裂原和应激激活的蛋白激酶1（mitogen-and stress-activated protein kinase 1，MSK1）在脑低氧预适应（HPC）发生发展过程中的作用。方法：按我们已建小鼠整体HPC模型，将健康成年BALB／c小鼠（18～22g，雄性）随机分为正常对照（H0）、早期（H1-H4）和延迟性（H5-H6）HPC等7组（每组n=6）。应用SDS-PAGE和Western blot技术，并结合Gel Doc凝胶成像系统，定量检测小鼠脑海马和皮层组织内MSK1第645位苏氨酸（p-Thr645-MSK1）和第375位丝氨酸（p-Ser375-MSK1）的磷酸化水平，以及MSK1总蛋白表达量的变化。结果：在脑早期（H1-H4）和延迟性（H5-H6）HPC形成过程中，随重复性低氧暴露次数的增加，H1-H6组小鼠海马和皮层组织内p-Thr645-MSK1及p-Ser375-MSK1的磷酸化水平较正常对照组（H0）显著增高（P〈0．05）；然而，小鼠海马和皮层组织内MSK1总蛋白表达量在H0-H6组中无明显变化。结论：MSKI磷酸化水平增高可能参与了小鼠脑HPC的发生发展过程。

英文摘要：

Objective： To explore the role of mitogen- and stress-activated protein kinase 1 （MSK1） in the development of cerebral hypoxic preconditioning. Methods： Using our established ＂Auto-hypoxia＂-induced I/HPC mouse model, which were conducted in healthy adult male BALB/c mice weighing 18-20g and ran domly divided into 7 groups （n=6 for each group） under repetitive hypoxic exposures （H 1-H6）. The groups were designed as follows： normoxic control （H0）, early （H1-H4） and delayed hypoxic preconditioned （H5 and H6） mice. The biochemical techniques of SDS-PAGE and Western blot combining with Gel Doc imaging system were applied to quantitatively analyze the changes in phosphorylations of MSK1 at Thr645 and Ser375, and to tal MSK1 protein expression both in hippocampus and cortex of mice. Results： In the development of cerebral I/HPC at early （H1-H4） and delayed （HS-H6） phases, the phosphorylation levels of MSK1 at both Thr645 and Ser375 increased significantly （P〈0.05） in hippocampus and cortex of mice in response to repetitive hypoxic exposures when we compared with that of H0 groups. However, there were no significant changes in total MSK1 protein expression levels both in the hippocampus and cortex of mice following repetitive hypoxic exposures （H1-H6）. Conclusions： Increased phosphorylations of MSK1 at Thr645 and Ser375 might be involved in the development of cerebral hypoxic preconditioning of mice.