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首页> 外文期刊>BMC Neuroscience >Enhanced cerebrovascular expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 via the MEK/ERK pathway during cerebral ischemia in the rat
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Enhanced cerebrovascular expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 via the MEK/ERK pathway during cerebral ischemia in the rat

机译：大鼠脑缺血期间通过MEK / ERK途径增强基质金属蛋白酶-9和金属蛋白酶-1组织抑制剂在脑血管中的表达

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Background Cerebral ischemia is usually characterized by a reduction in local blood flow and metabolism and by disruption of the blood-brain barrier in the infarct region. The formation of oedema and opening of the blood-brain barrier in stroke is associated with enhanced expression of metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Results Here, we found an infarct volume of 24.8 ± 2% and a reduced neurological function after two hours of middle cerebral artery occlusion (MCAO), followed by 48 hours of recirculation in rat. Immunocytochemistry and confocal microscopy revealed enhanced expression of MMP-9, TIMP-1, and phosphorylated ERK1/2 in the smooth muscle cells of the ischemic MCA and associated intracerebral microvessels. The specific MEK1/2 inhibitor U0126, given intraperitoneal zero or 6 hours after the ischemic event, reduced the infarct volume significantly (11.8 ± 2% and 14.6 ± 3%, respectively; P Conclusion These data are the first to show that the elevated vascular expression of MMP-9 and TIMP-1, associated with breakdown of the blood-brain barrier following focal ischemia, are transcriptionally regulated via the MEK/ERK pathway.
机译：背景技术脑缺血的特征通常在于局部血流和代谢的减少以及梗塞区域中血脑屏障的破坏。脑卒中水肿的形成和血脑屏障的开放与金属蛋白酶9（MMP-9）和金属蛋白酶-1（TIMP-1）的组织表达增强有关。结果在这里，我们发现梗死24.8±2％，大脑中部动脉闭塞2小时（MCAO）后再行48小时大鼠的神经功能降低。免疫细胞化学和共聚焦显微镜显示缺血性MCA和相关脑内微血管的平滑肌细胞中MMP-9，TIMP-1和磷酸化ERK1 / 2的表达增强。缺血事件后腹膜内零或6小时给予特定的MEK1 / 2抑制剂U0126，可显着减少梗死面积（分别为11.8±2％和14.6±3％; P结论）这些数据是第一个显示血管升高的数据MMP-9和TIMP-1的表达与局灶性缺血后血脑屏障的破坏有关，是通过MEK / ERK途径进行转录调控的。

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