| Summary: | 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.
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