PKC-MARCKS信号转导系统在急性多发脑梗死大鼠海马中的作用
he role of PKC-MARCKS signal transduction pathway in rats hippocampus with acute multi-cerebral infarction
目的 研究急性多发脑梗死大鼠海马MARCKS磷酸化动态变化与急性缺血损害的关系。方法 采用改良Kaneko法建立急性多发脑梗死动物模型，观察模型1h、6h、24h、72h、7d组大鼠海马病理组织学改变，应用免疫组织化学和Western blotting方法检测缺血各时间点大鼠海马MARCKS磷酸化表达变化。结果 海马组织病理学以缺血24h后病理改变为著。急性缺血海马MARCKS、p-MARCKS均为过高表达，24h表达最高，过表达最显著，24h后表达降低，7d表达略回升，形成动态变化。结论 急性多发脑梗死大鼠海马24h后缺血损害明显，24h海马MARCKS磷酸化过表达最显著，在急性脑缺血状态下大鼠海马MARCKS磷酸化过高表达，与缺血损害关系密切。
IM: To study the relationship between the alteration of hippocampus MARCKS phosphorylation and acute ischemia damage in rats hippocampus with acute multi-cerebral infarction.. METHODS: The acute multi-cerebral infarction model was established by method of Kaneko. The consequences of cerebral ischemic damage were examined by histopathological analyses. The changes of MARCKS phosphorylation expression was surveyed by immuno-histochemistry method and western blot technic. RESULTS: The hippocampus damage of histopathology became significant after ischemia 24h. The MARCKS、p-MARCKS overexpression at the area of rats hippocampus during ischemia. The hippocampus damage became significant after ischemia 24h. At the same time, MARCKS、p-MARCKS was a dynamic alteration. CONCLUSION: After 24h, the ischemic damage is obvious in rats hippocampus with acute multi-cerebral infarction. In 24h, hippocampus phosphorylation is remarkable overexpressed. The overexpression is strong related with ischemia damage in rats hippocampus with acute cerebral infarction.
张綦慧、韩振蕴、张允岭、闫妍、白文、张锦、郑宏、娄金丽
基础医学神经病学、精神病学
急性多发脑梗死大鼠海马MARCKS磷酸化
acute multi-cerebral infarctionrats hippocampusMARCKSphosphorylation
张綦慧,韩振蕴,张允岭,闫妍,白文,张锦,郑宏,娄金丽.PKC-MARCKS信号转导系统在急性多发脑梗死大鼠海马中的作用[EB/OL].(2007-12-26)[2025-08-18].http://www.paper.edu.cn/releasepaper/content/200712-704.点此复制
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