美诺环素对沙鼠脑缺血再灌注模型的神经保护作用机制研究  

To Study the Protective Effect of Minocycline on the Model of the Cerebral Ischemia-reperfusion of Gerbils

作　　者：杨剑文[1] 胡治平[1] 

机构地区：[1]中南大学湘雅二院,长沙410015

出　　处：《医学研究杂志》2009年第4期49-52,共4页Journal of Medical Research

摘　　要：目的探讨美诺环素通过抑制P38促分裂原活化蛋白激酶(P38MAPK)途径在沙鼠脑缺血再灌注模型中神经保护作用机制。方法采用夹闭双侧颈总动脉的方法制作沙鼠脑缺血再灌注模型;在电镜下观察不同时间海马CA1区及额叶脑组织超微结构的变化;用免疫组织化学方法检测各组沙鼠脑内磷酸化P38MAPK的表达情况。结果①在电镜下观察随着缺血再灌注的时间延长神经元损伤逐渐加重,美诺环素干预组明显减轻;②美诺环素干预组磷酸化P38MAPK表达趋势同缺血再灌注组,但其表达明显低于缺血再灌注组,差异有显著性(P<0.05)。结论美诺环素可能通过抑制P38促分裂原活化蛋白激酶(P38MAPK)途径保护神经元。Objective To explore the protective effect mechanism of minocyline on the model of the cerebral ischemia - reperfusion of gerbils by decreasing expression of phosphorylation P38MAPK. Methods A cerebral isehemla - reperfusion model in gerbils was established by clamping both common carotids. The ultrastructural alteration in pyramidal neuron in the hippocampal CA1 and the cortex of frontal lobe at different time was observed by electron microscope. And observe the expression level of phosphorylation P38MAPK by using immunohistochemistry technique. Results ①The damage to the neunos became more and more severe as gerbils survived longer postocelusion. Minocyline treated groups were lessened obviously. ② Treatment with minocycline reduced expression of phosphorylation P38MAPK with a significant difference（P 〈 0.05）. Conclusion Minocycline may exert neuroprotection by decreasing expression of phosphorylation P38MAPK.

关 键 词：脑缺血再灌注 美诺环素 磷酸化 P38MAPK 

分 类 号：R277.733[医药卫生—中医学] R285.5