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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Release of bradykinin and expression of kinin B2 receptors in the brain: role for cell death and brain edema formation after focal cerebral ischemia in mice.
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Release of bradykinin and expression of kinin B2 receptors in the brain: role for cell death and brain edema formation after focal cerebral ischemia in mice.

机译：缓激肽的释放和激肽B2受体在脑中的表达：在小鼠局灶性脑缺血后对细胞死亡和脑水肿形成的作用。

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摘要

Pharmacological studies using bradykinin B2 receptor antagonists suggest that bradykinin, an early mediator of inflammation and the main metabolite of the kallikrein-kinin system, is involved in secondary brain damage after cerebral ischemia. However, the time-course of bradykinin production and kinin receptor expression as well as the conclusive role of bradykinin B2 receptors for brain damage after experimental stroke have not been elucidated so far. C57/Bl6 mice were subjected to 45 mins of middle cerebral artery occlusion (MCAO) and 2, 4, 8, 24, and 48 h later brains were removed for the analysis of tissue bradykinin concentration and kinin B2 receptor mRNA and protein expression. Brain edema, infarct volume, functional outcome, and long-term survival were assessed in WT and B2-/- mice 24 h or 7 days after MCAO. Tissue bradykinin was maximally increased 12 h after ischemia (three-fold), while kinin B2 receptor mRNA upregulation peaked 24 to 48 h after MCAO (10- to 12-fold versus naive brain tissue). Immunohistochemistry revealed that kinin B2 receptors were constitutively and widely expressed in mouse brain, were upregulated 2 h after ischemia in cells showing signs of ischemic damage, and remained upregulated in the penumbra up to 24 h after ischemia. B2-/- mice had improved motor function (P<0.05), smaller infarct volumes (-38%; P<0.01), developed less brain edema (-87%; P<0.05), and survived longer (P<0.01) as compared with wild-type controls. The current results show that bradykinin is produced in the brain, kinin B2 receptors are upregulated on dying cells, and B2 receptors are involved in cell death and brain edema formation after experimental stroke.
机译：使用缓激肽B2受体拮抗剂的药理研究表明，缓激肽是炎症的早期介质，是激肽释放酶激肽系统的主要代谢产物，与脑缺血后继发性脑损伤有关。然而，到目前为止，尚不阐明缓激肽产生和激肽受体表达的时程以及缓激肽B2受体对实验性中风后脑损伤的决定性作用。对C57 / B16小鼠进行45分钟的大脑中动脉闭塞（MCAO），然后在2、4、8、24和48小时后取出大脑，以分析组织缓激肽浓度，激肽B2受体mRNA和蛋白表达。在MCAO后24小时或7天，对WT和B2-/-小鼠的脑水肿，梗塞体积，功能结局和长期存活率进行了评估。缺血后12 h，组织缓激肽最大增加（三倍），而MCAO后24至48 h，激肽B2受体mRNA上调达到峰值（相对于幼稚的脑组织，激肽B2受体mRNA上调至10至12倍）。免疫组织化学显示激肽B2受体在小鼠脑中组成性和广泛表达，缺血后2小时在表现出缺血性损伤迹象的细胞中上调，而在半影中直至缺血后24小时仍上调。 B2-/-小鼠具有改善的运动功能（P <0.05），较小的梗塞体积（-38％; P <0.01），较少的脑水肿（-87％; P <0.05）和存活时间更长（P <0.01）与野生型对照相比。目前的结果表明，大脑中会产生缓激肽，激肽中的激肽B2受体上调，实验性卒中后B2受体参与细胞死亡和脑水肿的形成。

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