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

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 ischemicdurations (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.