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降钙素基因相关肽对局灶性脑缺血再灌注大鼠海马tau磷酸化影响 被引量：1

Effect of CGRP on Tau Hyperphosphorylation in Rat Hippocampus after Focal Cerebral Ischemia-Reperfusion
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摘要 目的探讨降钙素基因相关肽(CGRP)对局灶性脑缺血再灌注大鼠海马神经元tau蛋白过度磷酸化的影响。方法应用免疫组织化学SABC法、Western Blotting和图像分析方法检测局灶性脑缺血再灌注大鼠海马CA1区tau蛋白在Ser199/202位点磷酸化程度和总tau蛋白表达、以及CGRP对缺血神经元tau蛋白过度磷酸化的影响。结果缺血再灌注大鼠海马CA1区tau蛋白在Ser199/202位点磷酸化水平和总tau表达水平明显增高,CGRP治疗后tau蛋白磷酸化水平和总tau表达水平明显低于缺血再灌注组(P<0.05)。结论CGRP明显减轻局灶性脑缺血再灌注大鼠海马tau蛋白磷酸化程度和总tau表达水平,可能对缺血神经元起保护作用。 Objective To explore the effect of exogenous calcitonin gene related peptide （CGRP） on tau hyperphosphorylation in rat hippocampus during focal cerebral ischemia/reperfusion （I/R）. Methods Focal cerebral ischemia/reperfusion model was induced by occlusion of the right middle cerebral artery using the intraluminal suture method. The levels of tau hyperphosphorylation at Ser199/202 site and total tau in rat ipsilateral hippocampus during focal cerebral ischemia/reperfusion were detected by immunohistochemical SABC method and Western Blotting. The immunoreactive positive products were analyzed by image analysis system. Results The levels of tau protein hyperphosphorylation at Ser199/202 site and total tau protein in rat hippocampal CA1 region were significantly higher in I/R group than in sham group （P〈0.05）. CGRP significantly reduced the levels of tau protein hyperphosphorylation at Ser199/202 site and total tau protein. Conclusion CGRP can attenuate the tau hyperphosphorylation and the level of total tau protein in rat hippocampus during focal cerebral ischemia-reperfusion. Inhibition of tau hyperphosphorylation may be involved in the protective mechanism of CGRP to ischemic neuron.
作者 张正洪 彭新民 杨龙珍 席刚明 周少华 尤志君 方秀斌
机构地区 郧阳医学院附属人民医院神经内科解剖学教研室 郧阳医学院药护学院 中国医科大学神经生物学教研室
出处 《解剖科学进展》 CAS 2008年第2期201-204,共4页 Progress of Anatomical Sciences
基金 湖北省教育厅重点项目(No.D20082407) 十堰市科技攻关计划项目(2007十科发19号)
关键词 降钙素基因相关肽 脑缺血 TAU蛋白 磷酸化 大鼠 Calcitonin gene related peptide cerebral ischemia tau protein phosphorylation rat
分类号 R743 [医药卫生—神经病学与精神病学] R322.81 [医药卫生—人体解剖和组织胚胎学]
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参考文献10

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共引文献10

同被引文献16

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