丁基苯酞对脑缺血模型谷氨酸兴奋性毒性作用的调控机制  

The mechanism of Butylphthalide protection against Glutamate excitotoxicity in MCAO rats

作　　者：赵慧颖 黄昕艳[2] 李航 闵程 郑勇骐 闫畅 郭淼 戚询中[4] 朱晓峰 ZHAO Hui-ying(Jiamusi University,Jiamusi 154000,China)

机构地区：[1]佳木斯大学 [2]佳木斯大学附属第二医院,黑龙江佳木斯154000 [3]伊春市林业中心医院,黑龙江伊春153000 [4]佳木斯大学附属第一医院,黑龙江佳木斯154000 [5]牡丹江医学院,黑龙江牡丹江157011

出　　处：《牡丹江医学院学报》2022年第4期44-47,共4页Journal of Mudanjiang Medical University

基　　金：国家重点研发计划项目(2018YFC1314404);黑龙江省教育厅基本科研业务费人才培养项目(2019-KYYWF-1357)。

摘　　要：目的分析丁基苯酞治疗缺血性脑血管疾病的作用机制。方法选用6~7周龄SD雄性大鼠,随机分为三组,Sham组(假手术组),MCAO组(采用Longa线栓法构建大脑中动脉阻塞模型)和NBP组(采用Longa线栓法构建大脑中动脉阻塞模型后使用丁基苯酞灌胃100 mg/kg,1次/d,共7 d);采用Zea Longa 5等级评分法对干预前后大鼠进行神经功能评分;采用实时荧光定量PCR及Western blot检测技术检测兴奋性氨基酸转运体1(Excitatory amino acid transporter1,EAAT1)、兴奋性氨基酸转运体2(Excitatory amino acid transporter2,EAAT2)表达,应用实时荧光定量PCR检测AKT mRNA变化。结果NBP组Zea Longa评分(1.467±0.516)较MCAO组大鼠模型(1.933±0.703)明显降低(P<0.05);NBP组EAAT1 mRNA(1.776±0.288)及蛋白表达(1.405±0.120)较MCAO组mRNA(1.389±0.266)及蛋白表达(1.124±0.127)升高(P<0.05);NBP组EAAT2 mRNA(1.663±0.269)及蛋白表达(0.580±0.142)较MCAO组mRNA(1.318±0.247)及蛋白表达(0.880±0.167)升高(P<0.05);NBP组AKT mRNA(1.462±0.303)较MCAO组AKT mRNA(1.041±0.306)明显升高(P<0.05)。结论丁基苯酞能够改善MCAO模型大鼠神经功能评分,促进模型大鼠皮质EAAT1和EAAT2的表达,同时活化PI3K/AKT途径,提高AKT mRNA水平,发挥神经保护作用。Objective To investigate the mechanism of Butylphthalide protection against Glutamate excitotoxicity in the middle cerebral artery occlusion(MACO)rats brain tissue.Methods A total of SD rats aged 6~7 weeks was divided into three groups:Sham group(Sham-operation group),MCAO group(The model of middle cerebral artery occlusion was established by Longa's method)and NBP group(The model of middle cerebral artery occlusion was established by Longa's method with NBP treatment(100 mg/(kg·d)by gavage,for 7 days).Then Zea Longa 5-grade scoring method was used to assess the neural function of experimental rats.The production levels of EAAT1(Excitatory Amino Acid Transporter 1)and EAAT2(Excitatory Amino Acid Transporter 2)were detected by qRT-PCR and Western blot,and the expressions of AKT in the cortex tissues were observed.Results Zea Longa score in NBP group(1.467±0.516)was significantly lower than that in MCAO group(1.933±0.703)(P<0.05).The mRNA(1.776±0.288)and protein(1.405±0.120)expressions of EAAT1 in NBP group were higher than those[mRNA(1.389±0.266)and protein(1.124±0.127)]in MCAO group(P<0.05).The mRNA(1.663±0.269)and protein(0.580±0.142)expressions of EAAT2 in NBP group were higher than those[mRNA(1.318±0.247)and protein(0.880±0.167)]in MCAO group(P<0.05).The mRNA(1.462±0.303)expressions of AKT in NBP group was significantly higher than that in MCAO group(1.041±0.306)(P<0.05).Conclusion NBP treatment could significantly improve motor function impairment induced by ischemia injury,increased the expression levels of EAAT1,EAAT2 and AKT,and play a protective role against cortex damage in MCAO rats.

关 键 词：丁基苯酞 MCAO大鼠模型 EAAT1 EAAT2 AKT 

分 类 号：R743.3[医药卫生—神经病学与精神病学]