The effects of dexamethasone treatment on blood-brain barrier of brain in intracerebral hemorrhage rat

• Main Authors: Chia-Hui Kuo, 郭佳惠
• Other Authors: none
• Format: Others
• Language: zh-TW
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/80221072882289180500

碩士 === 嘉南藥理科技大學 === 生物科技系暨研究所 === 95 === Intracerebral hemorrhage (ICH), an acute neurological disorder, has a rapidly evolving process that may progress over hours and days. The mechanisms of brain insult after ICH remain to be clarified. Matrix metalloproteinases (MMPs) is a family of zinc-dependent proteases which are involved in the degradation of basal lamina and extracellular matrix components. Although a few studies suggested a detrimental role of MMP-2 and MMP-9 in ICH, the relationships between it’s activity and the secondary brain changes after ICH are not determined. The intercellular adhesion molecule-1 (ICAM-1) binds to its leukocyte ligands and allows activated leukocytes entry into the CNS. In this study, we examine the expression of MMP-2, MMP-9 and ICAM-1 in vivo using a collagenase-induced rat model of ICH. Immunohistochemistry and Western blot revealed that MMP-2, MMP-9 and ICAM-1 was upregulated after ICH. The treatment with a broad-spectrum inflammation inhibitor dexamethasone (DEX) (15 mg/kg) could cause a decrease of MMP-2, MMP-9 and ICAM-1 expression and local neutrophil infiltration, then prevented the neuron death. The block of local brain edema around ICH was also observed. In conclusion, MMP-2, MMP-9 and ICAM-1 play a deleterious role in acute brain injury after ICH. The inhibition of MMP-2, MMP-9 and ICAM-1 expression with DEX during this critical period may be useful in treatment of secondary brain edema, which could be a therapeutic strategy for ICH.