褪黑素对IP诱导Tau过度磷酸化的保护作用  

Protection of isoproterenol-induced melatonin on hyperphosphorylation of tau

作　　者：凌智群[1] 廖晓梅[1] 王建枝[1] 

机构地区：[1]华中科技大学同济医学院病理生理教研室,湖北武汉430030

出　　处：《华中科技大学学报（自然科学版）》2004年第2期86-88,共3页Journal of Huazhong University of Science and Technology(Natural Science Edition)

摘　　要：通过对大鼠海马双侧注射异丙肾上腺素 (IP)或同时注射褪黑素 ( 0 .1μg,1μg) ,利用免疫组化、免疫印迹和Morris水迷宫等指标 ,在整体上观察褪黑素对IP诱导的骨架蛋白Tau过度磷酸化和动物保留记忆损伤的保护作用 .结果显示 0 .1μg和 1μg剂量的褪黑素能明显降低IP引起的海马骨架蛋白TauSer396 / 40 4位点的过度磷酸化 ;1μg褪黑素可明显改善IP引起的动物保留记忆损伤 。To study the in vivo effect of melatonin(MEL) on Alzh ei mer-like tau hyperphosphorylation and spatial memory retention impairment induc ed by isoproterenol (IP), IP (10?mM) or IP plus MEL(0.1?μg, 1?μg) was injec ted simultaneously into rat hippocampus bilaterally by stereotexin. The phosphor ylation of tau was analyzed by immunohistochemistry and western blot. The memory retention was tested by Morris Water Maze. The results showed that the injectio n of IP induced hyperphosphorylation of tau at Tau-1 and PHF-1 epitopes and in creased latency of rats to find the hidden platform in the Morris Water Maze. ME L significantly restored the IP-induced impairment in spatial memory (p<0. 05) and tau hyperphosphorylation determined both by immunohistochemistry and We stern blot. It was shown that MEL could inhibit partially the IP-induced pathol ogical processes in tau hyperphosphorylation and spatial memory impairment in ra t brain.

关 键 词：褪黑素 骨架蛋白Tau (-)异丙肾上腺素 

分 类 号：R363[医药卫生—病理学]