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首页> 外文期刊>Brain research >Inducible cyclooxygenase-2 expression after experimental intracerebral hemorrhage.
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Inducible cyclooxygenase-2 expression after experimental intracerebral hemorrhage.

机译：实验性脑出血后可诱导的环氧合酶2表达。

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Cyclooxygenase-2 (COX-2) is an inducible isoform of cyclooxygenase, which catalyzes the conversion of arachidonic acid to prostaglandins and thromboxane. Recent evidence suggests it has a pathological role in cerebral insults, but its involvement in intracerebral hemorrhage (ICH) is unknown. The present study investigates the temporal and anatomic distribution of COX-2 as well as the effect of the selective COX-2 inhibitor NS-398 on brain edema formation and cerebral blood flow in a rat model of ICH. Immunohistochemistry for COX-2 was performed in control rats and 6 h, as well as 1, 3, 7 and 10 days after the injection of 100 microl autologous blood into the right basal ganglia. Double-labeling immunohistochemistry was used to determine the type of COX-2 immunoreactive microvascular-associated cells. Western blot analysis was used to quantify COX-2 protein. The effect of NS-398 on brain water content, ion concentration and cerebral blood flow were assessed 24 h after ICH. The results demonstrated that COX-2 protein was expressed in control brain tissue and induced significantly in the ipsilateral hemisphere at 6 h, as well as 1 and 3 days after ICH. Increased staining of COX-2 in neurons was observed around the blood clot with a peak at 6 h. COX-2 was induced in endothelial cells, perivascular cells as well as infiltrating leukocytes 1 day after ICH. Brain water and ion contents and cerebral blood flow were unaffected by NS-398 administration. Thus, although COX-2 expression was increased in the ipsilateral hemisphere after an autologous blood injection, its products do not appear to be major regulators of blood flow or edema formation following ICH.
机译：环氧合酶2（COX-2）是环氧合酶的可诱导同工型，可催化花生四烯酸转化为前列腺素和血栓烷。最近的证据表明，它在脑损伤中具有病理作用，但其与脑出血（ICH）的关系尚不清楚。本研究调查了ICH大鼠模型中COX-2的时间和解剖分布以及选择性COX-2抑制剂NS-398对脑水肿和脑血流的影响。在对照组大鼠中以及在将100微升自体血注入右基底神经节后的6小时以及1、3、7和10天，进行了COX-2的免疫组织化学。使用双标记免疫组织化学确定COX-2免疫反应性微血管相关细胞的类型。 Western印迹分析用于定量COX-2蛋白。 ICH后24小时评估NS-398对脑含水量，离子浓度和脑血流量的影响。结果表明，COX-2蛋白在对照脑组织中表达，并在ICH后6 h以及ICH后1天和3天在同侧半球中被明显诱导。在血凝块周围观察到神经元中COX-2的染色增加，在6 h达到峰值。 ICH后1天，内皮细胞，血管周细胞以及浸润性白细胞中都诱导产生COX-2。 NS-398给药不影响脑水和离子含量以及脑血流量。因此，尽管自体血液注射后同侧半球中COX-2表达增加，但其产物似乎不是ICH后血流或水肿形成的主要调节剂。

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