中国组织工程研究

中国组织工程研究 ›› 2015, Vol. 19 ›› Issue (27): 4322-4327.doi: 10.3969/j.issn.2095-4344.2015.27.011

• 骨髓干细胞 bone marrow stem cells • 上一篇    下一篇

大鼠脑缺血模型中基质金属蛋白酶2/9活化增加及紧密连接蛋白逐渐降解

梁  佳1，戚智锋2，师文娟2，刘克建2   

  1. 1辽宁医学院科学实验中心，辽宁省锦州市  121001；
    2首都医科大学宣武医院脑血管病研究所，北京市  100053
  • 出版日期:2015-06-30 发布日期:2015-06-30
  • 通讯作者: 刘克建，教授首都医科大学宣武医院脑血管病研究所，北京市 100053
  • 作者简介:梁佳，女，1981年生，辽宁省锦州市人，汉族，实验师，辽宁医学院科学实验中心工作，主要从事脑血管病损伤与治疗方面的研究。
  • 基金资助:

    国家自然科学基金(81171242)；辽宁医学院校长基金项目资助(XZJJ20140105)

The increased activation of matrix metalloproteinase 2/9 and gradual degradation of claudin in rat models of middle cerebral artery ischemia 

Liang Jia1,Qi Zhi-feng2, Shi Wen-juan2, Liu Ke-jian2   

  1. 1Science Experimental Center of Liaoning Medical University, Jinzhou 121001, Liaoning Province, China; 
    2Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing 100053, Chin
  • Online:2015-06-30 Published:2015-06-30
  • Contact: Liu Ke-jian, Professor, Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing 100053, China
  • About author:Liang Jia, Studying for doctorate, Science Experimental Center of Liaoning Medical University, Jinzhou 121001, Liaoning Province, China
  • Supported by:

    the National Natural Science Foundation of China, No. 81171242; a grant from Principal Foundation of Liaoning Medical University of China, No. XZJJ20140105

PDF

378

被引次数

2

摘要：

背景：在脑卒中后急性期脑损伤过程中，基质金属蛋白酶破坏血管基膜的完整性，促进中性粒细胞和炎性因子的迁移，引起继发性脑损伤。
目的：观察大鼠局部脑缺血模型中不同缺血时间下基质金属蛋白酶2/9活性及紧密连接蛋白的降解规律。
方法：将39只雄性SD大鼠随机均分为3组，采用改良线栓法建立大脑中动脉缺血(脑卒中)模型，即分离颈外动脉，采用经颈外动脉插入线栓进入颈内动脉最终到达大脑中动脉的方法，3组缺血时间分别为3，5，7 h，再灌注后2 h，测试各组Zea-Longa和Ludmila Belayev神经功能学评分，脑组织梗死面积、基质金属蛋白酶2/9活性及紧密连接蛋白5的降解。
结果与结论：随着缺血时间的延长，脑梗死面积逐渐增大，组间两两比较差异有显著性意义(P < 0.05)；随着缺血时间的延长，中枢神经系统损伤逐渐加重，组间两两比较差异有显著性意义(P < 0.05)；随着缺血时间的延长，基质金属蛋白酶2/9的活性逐渐增强，组间两两比较差异有显著性意义(P < 0.05)；随着缺血时间的延长，紧密连接蛋白5的表达逐渐减少。说明长时间缺血后，脑组织的进行性损伤引起基质金属蛋白酶2/9活化的逐渐增加及紧密连接蛋白5的逐渐降解。

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

关键词: 实验动物, 脑及脊髓损伤动物模型, 脑缺血模型, 基质金属蛋白酶2, 基质金属蛋白酶9, 紧密连接蛋白5, 国家自然科学基金

Abstract:

BACKGROUND: During the process of acute brain injury after stroke, matrix metalloproteinase can undermine the integrity of vascular basement membrane, promote the migration of neutrophils and inflammatory factors, and cause secondary brain injury.
OBJECTIVE: To investigate the activation of matrix metalloproteinase 2/9 and the degradation rule of claudin in rat models of middle cerebral artery ischemia at different ischemic durations.
METHODS: Thirty-nine male SD rats were randomly divided into three groups according to different ischemic 
durations (3, 5 and 7 hours) . Middle cerebral artery occlusion (stroke) model was established using modified suture method, i.e., separation of the external carotid artery, inserting the suture into the internal carotid artery through the external carotid artery, and eventually reaching the middle cerebral artery. The ischemic duration in these three groups was respectively 3 , 5 and 7 hours. After 2 hours of reperfusion, Zea-Longa score and Ludmila Belayev score, brain infarct area, matrix metalloproteinase 2/9 activities and claudin 5 degradation were determined in each group.
RESULTS AND CONCLUSION: With the extension of ischemic duration, brain infarct area gradually increased, central nervous system damage gradually aggravated, matrix metalloproteinase 2/9 activities gradually increased, and claudin-5 expression gradually decreased. There were significant differences between any two ischemic durations in terms of each of above-mentioned indices. The results indicate that after long duration of ischemia, the progressive damage of brain tissue can cause the gradual increase of activation of matrix metalloproteinase 2/9 and the gradual degradation of claudin 5.

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

Key words: Cerebral Ischemia, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Claudin

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