The increased activation of matrix metalloproteinase 2/9 and gradual degradation of claudin in rat models of middle cerebral artery ischemia
10.3969/j.issn.2095-4344.2015.27.011
- VernacularTitle: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
- Author:
Jia LIANG
;
Zhifeng QI
;
Wenjuan SHI
;
Kejian LIU
- Publication Type:Journal Article
- Keywords:
Cerebral Ischemia;
Matrix Metaloproteinase 2;
Matrix Metaloproteinase 9;
Claudin
- From:
Chinese Journal of Tissue Engineering Research
2015;(27):4322-4327
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:During the process of acute brain injury after stroke, matrix metaloproteinase 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 metaloproteinase 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 eventualy 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 metaloproteinase 2/9 activities and claudin 5 degradation were determined in each group. RESULTS AND CONCLUSION:With the extension of ischemic duration, brain infarct area gradualy increased, central nervous system damage gradualy aggravated, matrix metaloproteinase 2/9 activities gradualy increased, and claudin-5 expression gradualy 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 metaloproteinase 2/9 and the gradual degradation of claudin 5.
