Inflammatory mediators and blood brain barrier disruption in fatal brain edema of diabetic ketoacidosis
Inflammatory mediators and blood brain barrier disruption in fatal brain edema of diabetic ketoacidosis
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DOI：
10.1016/j.brainres.2008.11.100
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发表时间：
2009-02-13
期刊：
影响因子：
2.9
通讯作者：
Andjelkovic, Anuska V.
中科院分区：
文献类型：
--
作者：
Hoffman, William H.;Stamatovic, Svetlana M.;Andjelkovic, Anuska V.
脑水肿（BE）是严重糖尿病酮症酸中毒（DKA）及其治疗的一种罕见但危及生命的并发症。尽管DKA的治疗取得了进展，但相关BE的发生和进展的发病机制尚不清楚。在本研究中，我们检查了血脑屏障（BBB）的完整性和潜在的参与血脑屏障破坏的炎症介质在两个案件的致命BE与DKA。在这两种情况下，存在典型的BBB破坏迹象，表现为实质血管中缺乏紧密连接蛋白（闭合蛋白、封闭蛋白-5、ZO-1和JAM-1），以及检查的脑区域中白蛋白外渗。神经炎性标志物趋化因子CCL 2、NF-κ B B和硝基酪氨酸定位于破坏的BB B的血管周围区域，并弥漫性分布于脑实质中。我们的数据表明，神经炎症在DKA致命BE的BBB破坏中发挥作用。(C)2008 Elsevier B. V.保留所有权利。
Brain edema (BE) is an uncommon but life-threatening complication of severe diabetic ketoacidosis (DKA) and its treatment. Despite advances in treatment of DKA, the pathogenesis of both initiation and progression of the associated BE is unclear. In the present study we examined the blood brain barrier (BBB) integrity and the potential involvement of the inflammatory mediators in BBB breakdown in two cases of fatal BE associated with DKA. in both cases there were typical signs of disruption of the BBB manifested by the absence of tight junction proteins (occludin, claudin-5, ZO-1 andJAM-1) in the parenchymal blood vessels, as well as albumin extravasation in examined brain areas. The neuroinflammatory markers chemokine CCL2, NF-kappa B and nitrotyrosine were localized in the perivascular areas of the disrupted BBB and diffusely distributed in the brain parenchyma. Our data indicate that neuroinflammation plays a role in the BBB disruption of the fatal BE of DKA. (C) 2008 Elsevier B.V. All rights reserved.