从缺血再灌大鼠皮层6-酮-前列腺素F_(1α)/血栓素B_2及血管内皮生长因子动态变化初探脑梗死络损机制  

Preliminarily investigating the collaterals damnif ication mechanism of cerebral infarction through detecting the dynamic expression of 6-Keto-PGF_(1α)/TXB_2 and VEGF in cerebral cortex of rats after cerebral ischemia reperfusion

作　　者：刘超[1] 张允岭[1] 陶冶[1] 刘雪梅[1] 娄金丽[1] 郑宏[1] 闫妍[1] 

机构地区：[1]北京中医药大学东方医院,北京100078

出　　处：《中华中医药杂志》2008年第5期386-388,共3页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：国家重点基础研究发展计划(973计划)项目(No.2006CB504805);教育部新世纪优秀人才支持计划(No.NCET-05-0139)

摘　　要：目的:从局灶缺血再灌大鼠皮层6-酮-前列腺素F1α(6-Keto-prostaglandin F1α,6-Keto-PGF1α)/血栓素B2(thromboxane B2,TXB2)、血管内皮生长因子(vascular endothelial growth factor,VEGF)动态变化,初步探讨脑梗死络损机制。方法:线栓法制备大鼠大脑中动脉脑缺血再灌注模型;用放射免疫法检测不同时间点患侧皮层6-Keto-PGF1α、TXB2含量及二者比值的变化;用免疫组织化学方法检测VEGF相关表达。结果:同假手术组比较,模型组6-Keto-PGF1α先呈下降趋势,于3h降至最低(P<0.05),随后上升,并于24h达到高峰(P<0.05);TXB2呈上升趋势,于24h达到高峰(P<0.01);二者比值呈下降趋势,且于3h最低(P<0.01);VEGF表达呈上升趋势,并于24h达到高峰(P<0.01)。结论:6-Keto-PGF1α/TXB2平衡失调是脑缺血损害的重要环节,VEGF参与缺血性脑损伤的病理发展和修复过程,以二者动态病理改变为代表的微循环灌流障碍可体现脑梗死络损机制。Objective：To preliminarily investigate the collaterals damnification mechanism of cerebral infarction through detecting the dynamic expression of 6-Keto-PGF1α/TXB2 and VEGF in cerebral cortex of rats after focal cerebral ischemia reperfusion. Methods： Rat models of focal cerebral ischemia and reperfusion were established by thread ligation in middle cerebral artery . The levels of 6-Keto-PGF1α and TXB： of cerebral cortex at different time point were measured by radioimmunoassay, and the expressions of VEGF were assayed by using immunohistochemical staining and image analysis. Result： Compared with the sham group, the model group 6-Keto-PGF1α began to decrease after reperfusion at first, and reach the lowest at 3h （P〈0.05）,then began to increase and reach peak at 24h （P〈0.05）. TXB2 concentration obviously increased and reach peak at 24 h （P〈0.01）. 6-Keto-PGF1α/TXB2 ratio markedly decreased and reach the lowest at 3h. VEGF obviously increased and reach peak at 24h（P〈0.01）. Conclusion：The disequilibrium of 6-Keto-PGF1α and TXB2 is a important point of the pathological lesion of cerebral ischemia, VEGF participates the pathological lesion and reparative process of cerebral ischemia, and the disorder of microcirculation, which represented by those dynamic pathological changes ,can reflect the collaterals damnification mechanism of cerebral infarction.

关 键 词：脑缺血再灌 前列环素 血栓素B2 血管内皮生长因子 络损 实验研究 

分 类 号：R277.7[医药卫生—中医学]