摘要
目的:通过建立大鼠慢性脑低灌注模型,观察慢性脑低灌注状态下正常脑灌注压恢复过程中P21和P53蛋白的表达情况。方法:实验于2003-12/2004-12在锦州医学院动物实验中心进行。取Ⅱ级Wistar雄性大鼠60只,随机分为对照组、模型不灌注组和模型再灌注组:每组动物按正常灌注压恢复后不同时间点分组(12,24,48,72h组),每个时间点各5只。采用右侧颈外静脉-颈总动脉端侧吻合和对侧横窦引流静脉结扎的方法,建立慢性脑低灌注动物模型,术后90d阻断颈部动静脉分流造成模型组大鼠脑组织再灌注。各组在恢复正常灌注后12,24,48,72h取材,应用免疫组化和显微图像分析方法检测慢性脑低灌注状态下正常脑灌注压恢复过程中大鼠海马P21和P53蛋白的表达。结果:P21和P53蛋白在对照组大鼠脑组织中无表达,48h灰度值分别为155.34±1.18和172.91±1.37;在模型不灌注组中弱表达,48hP21和P53蛋白分别为125.12±3.56和112.10±4.46;在模型再灌注组大鼠脑组织中P21和P53蛋白于术后12h开始有表达,48h达高峰,分别为53.32±2.84和54.12±0.34,随后逐渐降低。结论:慢性脑低灌注状态下,正常脑灌注压恢复过程中可诱导P21和P53蛋白的表达。
AIM:To establish a rat model of chronic cerebral hypoperfusion so as to investigate the expression of P21 and P53 protein following normal perfusion pressure restoration process. METHODS:The experiment was performed in the Animal Experimental Center of Jinzhou Medical College from December 2003 to December 2004.Totally 60 Wistar rats were randomly divided into control group,model group without reperfusion and model group with reperfusion assessed at various time points after reperfusion of normal perfusion pressure(12 hours,24 hours,48 hours,72 hours,n=5).Rats in model groups were accomplished by end to side anastomosis between the right external jugular vein and common carotid artery,as well as ligation of the left vein draining the transverse sinus and bilateral external carotid arteries.Three months later,occlusion of carotid jugular shunting resulted in reperfusion in rat brains of the model group.After normal perfusion,rats were detected at 12,24,48 and 72 hours.The expression of P21 and P53 protein during normal perfusion pressure restoration process in condition of chronic cerebral hypoperfusion was detected with immunohistochemical method and microimage analysis system. RESULTS:The expression of P21 and P53 protein in rat brain were not observed in control group,and the grey value wsa 155.34±1.18 and 172.91±1.37 at 48 hours, respectively.P21 and P53 protein levels were lowered in rat brain of the model group without reperfusion,and were 125.12±3.56 and 112.10±4.46 at 48 hours, respectively. However, P21 and P53 protein began to increase in rat brain of the model groups with reperfusion at 12 hours and peaked to the top(53.32±2.84, 54.12±0.34) at 48 hours, and then decreased. CONCLUSION:The results demonstrate that normal perfusion pressure restoration process can induce the expression of P21 and P53 protein following chronic cerebral hypoperfusion.
出处
《中国临床康复》
CSCD
北大核心
2005年第13期76-77,i004,共3页
Chinese Journal of Clinical Rehabilitation
