灯盏乙素对高血脂大鼠脑缺血再灌注损伤的影响及机制

Effects and mechanisms of scutellarin on cerebral ischemia-reperfusion injury in rats with hyperlipemia

目的:研究灯盏乙素对高血脂大鼠脑缺血再灌注损伤的影响,并探讨其机制。方法:喂养高脂饲料建立大鼠高血脂模型,线栓阻塞大脑中动脉复制大鼠脑缺血恢复血流后的再灌注损伤模型,随机分为假手术组、生理盐水对照组和灯盏乙素干预组,灯盏乙素干预组在再灌注开始时及再灌注12h时由尾静脉注射灯盏乙素注射液(4ml/kg),同时其他2组注射等剂量的生理盐水。神经功能学评分观察大鼠的神经功能变化,TTC染色观察大鼠的脑坏死灶大小变化,伊文思蓝染色观察大鼠血脑屏障的通透性变化,免疫印迹和RT-PCR观察大鼠大脑皮层内基质金属蛋白酶9(MMP-9)及MMP-9mRNA的表达变化。结果:再灌注24h时,与生理盐水对照组相比,灯盏乙素干预组MMP-9及MMP-9mRNA的表达水平、神经功能学评分、脑坏死灶大小、血脑屏障的通透性均降低,差异有统计学意义。结论:高血脂脑缺血大鼠恢复血流后的再灌注损伤中,灯盏乙素可通过抑制MMP-9的表达,从而减轻脑组织的再灌注损伤。

Objective:To investigate the effect of scutellarin on cerebral ischemia-reperfusion injury in rats with hyperlipemia and to explore its mechanism.Methods:The rat model of hyperlipidemia was established by high-fat feeding.The cerebral ischemia-reperfusion model was established with thread embolism of the middle cerebral artery.The rats were randomly divided into sham operation group,normal saline control group and scutellarin intervention group.In the scutellarin intervention group,scutellarin injection(4 ml/kg)was injected into the tail vein at the beginning of reperfusion and 12 h after reperfusion.At the same time,the other two groups were injected with equal doses of normal saline.Neurofunctional score was used to observe the neurofunctional changes.TTC staining was used to observe the focal cerebral necrosis.Evans blue staining was used to detect the blood-brain barrier permeability.Western blotting and reverse transcription PCR were used to examine the expressions of MMP-9 and MMP-9 mRNA in the cerebral cortex of rats.Results:At 24 h after reperfusion,compared with saline group,the expressions of MMP-9 and MMP-9 mRNA,neurofunctional score,cerebral infarction volume and blood-brain barrier permeability were significantly decreased in scutellarin intervention group,and the results were significantly different.Conclusion:After cerebral ischemia-reperfusion injury in rats with hyperlipemia,scutellarin can alleviate cerebral ischemiareperfusion injury by inhibiting the expression of MMP-9.