脑血疏口服液对大鼠脑缺血再灌注损伤后血脑屏障的影响

The effects of Naoxueshu oral liquid on blood-brain barrier after cerebral ischemia-reperfusion injury in rats

目的探讨脑血疏口服液对大鼠脑缺血再灌注损伤后血脑屏障的影响。方法将120只SD大鼠随机分为3组:假手术组、对照组,脑血疏组;采用线栓法建立大鼠左侧大脑中动脉闭塞再灌注模型,缺血2 h后拔出线栓,恢复灌注24 h;采用Longa FZ 5级评分法进行大鼠神经功能缺损评分;TTC染色计算脑梗死体积百分比;运用干-湿重法测脑含水率;通过伊文思蓝(EB)含量反映血脑屏障的损伤程度;免疫组化检测基质金属蛋白酶-9(MMP-9)的表达水平。结果 (1)假手术组大鼠在神经功能缺损评分、脑梗死体积、脑含水率均低于对照组(P<0.01);脑组织中EB含量和MMP-9表达水平较对照组低(P<0.01);(2)脑血疏组大鼠的神经功能缺损评分较低、脑梗死体积较小,脑水肿程度较轻;EB含量和MMP-9表达水平均较对照组明显减少(P<0.01)。结论脑血疏口服液对大鼠脑缺血再灌注损伤后血脑屏障具有保护作用,其机制可能是通过抑制MMP-9的表达。

Objective To investigate the effects of Naoxuechu oral liquid on blood-brain barrier after cerebral ischemia-reperfusion injury in rats. Methods 120 SD rats were randomly divided among three groups： sham-operation group,control group and Naoxueshu group. The middle cerebral artery occlusion reperfusion model was established by thread embolism method. After 2 hours of ischemia,the suture was pulled out and the perfusion was resumed for 24 h. The neurological deficit was assessed by Longa FZ 5-score while TTC staining was utilized to calculate the percentage of cerebral infarct volume. The dry-wet weight method was used to measure the water content of the brain and the level of the blood-brain barrier was reflected by Evans blue（ EB） content. The expression of matrix metalloproteinase-9（ MMP-9） was considered by immunohistochemistry. Results Compared with the control group,the neurological deficit score,cerebral infarct volume and cerebral edema were significantly lower in the sham-operation group（ P〈0. 01）,and the EB content and MMP-9 expression in the brain tissue were less. The difference was significant（ P〈0. 01）. Compared with the control group,the scores of neurological deficits,cerebral infarction volume and cerebral edema were lower in Naoxueshu group. The content of EB and the expression of MMP-9 was significantly lower than those in the control group. There was considerable statistical difference（ P〈0. 01）. Conclusion Naoxueshu oral Liquid has the protective effect on the blood-brain barrier after cerebral ischemia reperfusion injury in rats. The mechanism might be through inhibition of MMP-9 expression.