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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Expression of Matrix Metalloproteinse-9 in Thrombin-Induced Brain Edema Formation in Rats
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Expression of Matrix Metalloproteinse-9 in Thrombin-Induced Brain Edema Formation in Rats

机译：凝血酶诱导的大鼠脑水肿形成过程中基质金属蛋白酶9的表达

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Recent evidence has demonstrated that thrombin plays an important role in the development of brain edema by the blood-brain barrier disruption in intracerebral hemorrhage. Matrix metalloproteinases (MMPs), a family of proteolytic enzymes that degrade the extracellular matrix, are implicated in blood-brain barrier disruption. In this study, we examined whether thrombin injection into the brain parenchyma induces the MMP-9 expression in rats. Anesthetized adult rats received an injection of 10 U of thrombin into the basal ganglia. At 12, 24, and 72 hours after the thrombin injection, brain water content and the expression of MMP-9 messenger RNA (mRNA) and protein were determined. The effect of a specific thrombin inhibitor (hirudin) on MMP-9 expression and brain edema formation and general administration of synthetic MMPs inhibitor (GM6001) on brain edema formation were also examined for linking the injury and up-regulation of MMP-9. The brain water contents in the basal ganglia and overlying cortex wererapidly increased at 12 hours, maximized at 24 hours, and slightly decreased at 72 hours. The gelatinase activity of MMP-9 determined with gelatin zymography was detected in the basal ganglia and cortex at 12 hours, maximally expressed at 24 hours, and remained strong 72 hours after thrombin injection. The expression of MMP-9 mRNA in the cortex determined with reverse transcription-polymerase chain reaction was clearly seen at 12 and 24 hours, and became weak 72 hours after thrombin injection. Co-injection of thrombin and hirudin almost completely inhibited the brain edema formation and expressions of MMP-9 mRNA and protein. Administration of broad-spectrum metalloproteinase inhibitor GM6001 significantly reduced the brain edema formation in this model. These results indicate that intraparenchymal thrombin induces brain edema formation through MMP-9 expression in rats. Inhibition of MMPs activity may provide an approach to potentially reduce ongoing edema after intracerebral hemorrhage. 2006 National Stroke Association.
机译：最近的证据表明，凝血酶通过脑出血中的血脑屏障破坏在脑水肿的发展中起重要作用。基质金属蛋白酶（MMP）是降解细胞外基质的蛋白水解酶家族，与血脑屏障破坏有关。在这项研究中，我们检查了向脑实质注射凝血酶是否会诱导大鼠中MMP-9的表达。麻醉的成年大鼠向基底神经节注射了10 U凝血酶。凝血酶注射后第12、24和72小时，测定脑含水量以及MMP-9信使RNA（mRNA）和蛋白质的表达。还检查了特定的凝血酶抑制剂（hirudin）对MMP-9表达和脑水肿形成的影响，以及合成MMPs抑制剂（GM6001）对脑水肿形成的一般给药与损伤和MMP-9上调的关系。基底神经节和上覆皮层中的脑水含量在12小时迅速增加，在24小时达到最大，而在72小时则略有下降。用明胶酶谱法测定的MMP-9的明胶酶活性在12小时时在基底神经节和皮质中检测到，在24小时时最大表达，并在凝血酶注射后72小时保持强势。通过逆转录-聚合酶链反应测定的皮层中MMP-9 mRNA的表达在12和24小时清晰可见，并且在凝血酶注射后72小时变得弱。凝血酶和水rud素的共同注射几乎完全抑制了脑水肿的形成以及MMP-9 mRNA和蛋白的表达。在此模型中，广谱金属蛋白酶抑制剂GM6001的使用显着减少了脑水肿的形成。这些结果表明实质内凝血酶通过大鼠MMP-9表达诱导脑水肿形成。 MMPs活性的抑制可能提供一种潜在的方法来减少脑出血后正在进行的水肿。 2006年全国中风协会。

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