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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,北京100069
出 处:《基础医学与临床》2007年第5期481-484,共4页Basic and Clinical Medicine
基 金:国家自然科学基金(30470650;30670782);北京市自然科学基金(07E0029);国家重点基础性研究项目(2006CB504100)
摘 要:目的探讨P38丝裂原激活蛋白激酶(mitogen.activatedproteinkinase,P38MAPK)在小鼠脑低氧预适应形成过程中的作用。方法用成年雄性BALB/c小鼠制备小鼠整体低氧预适应模型,小鼠随机分为正常对照(H0)、早期(H1~H4)和延迟性(F15~H6)低氧预适应等7组;应用Westernbolt并结合GelDoc凝胶成像系统,定量检测小鼠脑组织内P38MAPK磷酸化水平和蛋白表达量。结果与H0组小鼠相比,H2~H6组的海马和皮层及H3~H6组的下丘脑中P38MAPK磷酸化水平明显增高(P〈0.05,每组n=6);H1~H6组的皮层、海马和下丘脑中P38MAPK蛋白表达量无明显变化。结论P38MAPK磷酸化激活而非蛋白表达量的变化可能参与了小鼠脑低氧预适应的发生、发展过程。Objective To explore the role of P38 mitogen-activated protein kinase (P38 MAPK) in the development of cerebral hypoxic preconditioning. Methods Healthy male BALB/C mice weighted as18 ~ 20 g were randomly divided into 7 groups as follows: normoxic control (H0), early (H1 ~ H4) and delayed (H5 and H6) hypoxic preconditioned mice groups. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to quantitatively analyze the level of P38 MAPK phosphorylation and protein expression in the brain of mice. Results The phosphorylation levels of P38 MAPK increased in cortex, hippocampus and hypothalamus of mice in both early ( H1 ~ H4) and delayed ( H5 and H6) hypoxic preconditioned groups, and the statistic significance ( P 〈 0.05, n = 6 for each group) was recorded cortex and hippocampus of mice from H2 ~ H6, and hypothalamus of mice from H3 ~ H6 groups in comparison to H0 (n = 6), respectively. However, there was no significant changes in P38 MAPK protein expression in cortex, hippocampus and hypothalamus of hypoxic preconditioned mice from H1 ~ H6 groups when compared with H0 ( n = 6). Conclusion The increased phosphorylation (activation) of P38 MAPK but not protein expression, was be involved in the development of cerebral hypoxic preconditioning of mice.
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