朝鲜当归提取物对小鼠脑缺血-再灌注损伤神经的保护作用及其机制  

Neuroprotective Effects and Its Mechanism of Extract of Angelica gigas Nakai on Erebral Ischemia/Reperfusion Injury in Mice

作　　者：程永杰 赵子瑞[2] 李晓妮[2] 吉海杰[3] CHENG Yongjie;ZHAO Zirui;LI Xiaoni;JI Haijie(Department of Pharmacy,Shanxi Pharmaceutical Vocational College,Taiyuan 030031,China;College of Pharmacy,Shanxi Medical University,Taiyuan 030001,China;Shanxi Provincial Hospital of Traditional Chinese Medicine,Taiyuan 030012,China)

机构地区：[1]山西药科职业学院药学系,太原030031 [2]山西医科大学药学院,太原030001 [3]山西省中医药研究院,太原030012

出　　处：《医药导报》2020年第1期22-26,共5页Herald of Medicine

基　　金：国家自然科学基金资助项目(81603614)

摘　　要：目的探讨朝鲜当归提取物对小鼠脑缺血-再灌注(I/R)损伤影响及其机制。方法雄性C57BL/6小鼠随机分为6组,分别为假手术组、模型对照组和朝鲜当归(10,25,50,100 mg·kg-1)组(n=9)。I/R小鼠采用大脑中动脉阻塞(MCAO)方法使小鼠短暂缺血90 min,再灌注24 h。应用2,3,5-氯化三苯基四氮唑染色法和伊文思兰染色评价大鼠脑梗死体积和血-脑屏障通透性变化;利用蛋白免疫印迹(Western blotting)方法检测血管生成诱导蛋白如血管生成素1(Ang-1)和血管内皮生长因子(VEGF)表达,紧密连接蛋白如ZO-1和Occludin表达;同时检测磷脂酰肌醇3-激酶(PI3K)/Akt磷酸化表达。结果朝鲜当归提取物可显著缩小I/R小鼠脑梗死体积(P<0.05),降低I/R小鼠血-脑屏障通透性(P<0.05),还可激活PI3K/Akt通路,增加Ang-1、VEGF、ZO-1和Occludin蛋白表达(P<0.05)。结论朝鲜当归可能通过降低血脑屏障通透性及促进血管生成在小鼠I/R损伤中发挥神经保护作用。Objective To evaluate the effect and its mechanism of Angelica gigas(AG)extract on cerebral ischemia/reperfusion(I/R)injury in mice.Methods Male C57BL/6 mice were randomly divided into six groups(n=9):sham group,model control group and AG group(10,25,50,100 mg·kg-1).I/R mice were subjected to transient middle cerebral artery occlusion(MCAO),resulting in transient ischemia of 90 min and reperfusion of 24 h.After 24 h reperfusion,infarction volume and the changes of blood-brain barrier permeability were measured by 2,3,5-triphenyltetrazolium chloride(TTC)and Evans blue(EB)staining.The expression of angiogenesis-induced proteins,angiopoietin-1(Ang-1)and vascular endothelial growth factor(VEGF),tight junction proteins,ZO-1 and Occludin,and the phosphorylation of phosphatidylinositol 3-kinase(PI3K)/AKT were determined in the ischemic brains by Western blotting,respectively.Results The treatment of AG significantly decreased the volumes of brain infarction in I/R mice(P<0.05).AG decreased the permeability of blood-brain barrier comparing to I/R group(P<0.05).AG also significantly increased the expression of Ang-1,VEGF,ZO-1 and Occludin through activation of the PI3K/Akt pathway(P<0.05).Conclusion AG may play a neuroprotective role in I/R injury against mice by reducing blood-brain barrier permeability and promoting angiogenesis.

关 键 词：朝鲜当归 缺血-再灌注 脑 神经保护作用 

分 类 号：R282.71[医药卫生—中药学] R285.5[医药卫生—中医学]