摘要
目的:通过建立兔二次蛛网膜下腔出血实验模型,观察兔蛛网膜下腔出血后基底动脉缝隙连接蛋白Cx43表达与注血量的关系,初步探讨蛛网膜下腔出血量是否通过调节缝隙连接蛋白的表达参与脑血管痉挛的形成。方法:选择健康新西兰大白兔18只,随机分为3组:正常组和0.5mL注血组,1 mL注血组(每组n=6);建立兔二次蛛网膜下腔出血后脑血管痉挛实验模型,脑血管造影分析基底动脉的直径变化并应用Western Blot检测基底动脉Cx43蛋白的表达变化。结果:成功建立兔二次蛛网膜下腔出血模型;脑血管造影显示正常组7 d与0 d相比血管直径无明显变化(95.2±3.4)%,0.5 mL注血组7 d较0 d血管狭窄[(82.3±4.6)%,P<0.05],1 mL注血7 d较0d血管明显狭窄[(63.5±6.8)%,P<0.01]。Cx43蛋白表达在正常组为(33.9±6.1)%,0.5mL注血组为(53.4±3.5)%,(P<0.05)、1 mL注血组为(61.6±3.8)%,(P<0.01)。结论:实验结果显示蛛网膜下腔出血后兔基底动脉缝隙连接蛋白Cx43的表达与出血量成正比关系,表明蛛网膜下腔出血量的变化可能通过调节血管壁Cx43蛋白的表达参与脑血管痉挛的形成。
Objective：The study was designed to explore the change of expression connexin43 （Cx43） protein with different blood volume after the model of subarachnoid hemorrhage （SAH） in rabbits,which ,sill provide the SAH blood volume whether affeet the GJ function to form the mechanism of cerebral vasospasm （CVS）. Methods： 18 New Zealand rabbits were divided into 3 groups ：SAH group （blood volume 0.5ml, lml） and control group （n=6）.The mode/of CVS following SAH was established. Digital subtraction angiography was performed to detect the change of the basilar arteries diameter .The expression of Cx43 protien in basilar arteries tissue at different time points following experimental SAH was examined by using western blotting analysis. The data were statistieally analyzed using the Bivariate correlations test. Results ：The model of SAH in rabbits was successfully established. All 18 rabbits were analyzed. Cerebral angiograms on day 7 and day 0 showed no marked change diameter of the BAs in control group （95.2±3.4）% ,and in 0.5ml group is angiostegnosis [ （82.3±4.6）% ,P〈0.05], 1.0 group is obviously angiostegnosis [ （63.5±6.8）% ,P〈0.01 ] ,compared to normal group .western blotting showed that the expression of Cx43 protein were detected in normal rabbit basilar arteries tissue （33.9±6.1）%.However ,the experssion of Cx43 protein increased gradually in models and significantly compared with that of control [ （53.4±3.5） % , P 〈0.05 ], [ （61.6 ±3.8） % , P 〈0.01 ],There were positive correlations between expression of Cx43 and cerebral vasospasm. Conclusions ：The above results demonstrated of the first time that the Cx43 protein expression was altered with different blood volume after the SAH, and exhibited a blood volume-dependent change. SAH might be connected with the development of CVS. In summary,it demonstrated the blood volume aecording regulate gap junction protein expression to form in the pathogenesis of cerebral vasospasm after SAH.
出处
《赣南医学院学报》
2010年第2期186-188,共3页
JOURNAL OF GANNAN MEDICAL UNIVERSITY
基金
国家自然科学基金课题(30660188):缝隙连接重构参与脑血管痉挛的分子机制研究
