常压氧疗对大鼠脑缺血再灌注后血脑屏障损伤的作用及机制  

The effect and mechanism of normobaric hyperoxia on blood-brain barrier impairment following cerebral ischemia-reperfusion in rats

作　　者：刘宝义[1] 张晓明[2] 郭晓笋[2] 胡维诚[2] 袁中瑞[2] 

机构地区：[1]山东大学齐鲁医院呼吸内科,济南250012 [2]山东大学医学院病理生理学教研室,济南250012

出　　处：《山东大学学报（医学版）》2010年第12期27-31,共5页Journal of Shandong University:Health Sciences

基　　金：山东省自然科学基金资助项目(2009ZRB01125)

摘　　要：目的研究常压氧疗对大鼠脑缺血再灌注后血脑屏障损伤的作用及机制。方法采用大鼠大脑中动脉线栓法制备脑缺血再灌注模型。随机将30只SD雄性大鼠,分为模型对照组和常压氧疗治疗组各15只,缺血90min后再灌注24h。采用TTC染色、伊文思蓝法和明胶酶谱技术,分别检测脑梗死体积、血脑屏障通透性及缺血脑组织基质金属蛋白酶-9(MMP-9)的活性,并进行神经功能评分。结果与对照组比较,常压氧疗治疗组大鼠的脑梗死体积、缺血脑组织伊文思蓝外渗率及MMP-9的活性显著降低(P(0.01),神经功能缺陷也得到显著改善。结论缺血期内的常压氧疗对大鼠脑缺血再灌注后血脑屏障的损伤具有保护作用,其作用机制可能是通过抑制MMP-9的活性来实现的。Objective To investigate the effect of normobaric hyperoxia on blood brain barrier impairment following cerebral ischemia-reperfusion in rats,and explore the mechanism.Methods 30 normal male SD rats were randomly divided into 2 groups：① cerebral ischemia-reperfusion control group（n=15）,and ② normobaric hyperoxia treatment group（n= 5）.Cerebral ischemia-reperfusion rat models were established by thread ligation of the right middle cerebral artery.At 24 hrs after the reperfusion following 90 min ischemia,TTC staining,Evans blue dye extravasation and Gelatin zymography were applied to quantify infarction volume,blood-brain barrier impairment and the activity of MMP-9,respectively.Neurological deficit scores were also evaluated.Results Compared with the control group,normobaric hyperoxia treatment significantly decreased Evans blue dye extravasation,the activity of MMP-9 and infarct volume（P﹤0.01）at 24 hrs after the reperfusion.Correspondingly,neurological functions were improved.Conclusions Normobaric hyperoxia treatment during the period of focal cerebral ischemia demonstrates the protective effect on blood-brain barrier impairment in the rat model of cerebral ischemia-reperfusion,and the mechanism may be attributed to the suppression of MMP-9.

关 键 词：再灌注损伤 缺氧缺血 脑 血脑屏障 明胶酶B 大鼠 

分 类 号：R614.2[医药卫生—麻醉学] R332[医药卫生—外科学]