摘要
目的观察β-七叶皂甙钠对大鼠脑缺血再灌注损伤后血脑屏障功能和GFAP表达的影响,探讨其对脑缺血再灌注损伤的保护作用及其机制。方法 60只SD大鼠随机分为假手术组对照组β-七叶皂甙钠治疗组各20只。线栓法制作大鼠脑缺血再灌注模型,再灌注48h后干湿重法测定脑含水量,用伊文思蓝测定血脑屏障通透性,免疫组织化学技术检测GFAP的表达,同时电镜观察血脑屏障的变化。结果脑缺血再灌注48h,对照组缺血侧脑含水量明显升高,电镜观察发现血脑屏障破坏严重,GFAP的表达也较假手术组显著增加;而应用β-七叶皂甙钠处理的大鼠其缺血脑含水量明显减少,同时电镜观察到血脑屏障的破坏减轻,而GFAP表达水平也明显低于对照组(P<0.05)。结论β-七叶皂甙钠对大鼠脑缺血再灌注损伤后的血脑屏障具有保护作用,其机制可能与抑制GFAP表达,减轻脑水肿有关。
Objective To investigate the effect of β-aescinate sodium on blood-brain barrier of cerebral ischemia and reperfusion rats,and explore the mechanism of it.Methods 60 normal male SD rats were distributed randomly to 3 groups：①Sham-operation（n=20）;②Control（n=20）;③β-aescinate sodium（n=20）.Cerebral ischemia and reperfusion rat models were made using the method of thread inserting right middle cerebral artery occlusion（MCAO）,The brain water content were measured 48 h after reperfusion.At the same time,The permeability of blood-brain barrier was observed with electron microscope and by detecting the content of Evans Blue leaked out the brain tissue of ischemic side.The expression of GFAP in different groups was detected by immunohistochemical method.Results 48 h after crebral ischemia and reperfusion injuries,the content of brain water and Evans Blue leaked out the brain tissue of ischemic side increased obviously,The breakdown of blood-brain barrier was severe on electron microscope,the expression of GFAP also increased obviously.However,β-aescinate sodium can subtract the content of brain edema and Evans blue（P0.05）,relieve the breakdowm of blood-brain barrier on electron microscope.The expression of GFAP were decreased in β-aescinate sodium group contrasted with control group（P0.05）.Conclusion β-aescinate sodium has the protective effect on BBB in the model rats of cerebral ischemia and reperfusion injuries.The mechanism may be by restrainning the expression of GFAP and relieving brain edema.
出处
《四川医学》
CAS
2010年第10期1429-1432,共4页
Sichuan Medical Journal
