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首页> 外文期刊>Translational Stroke Research >Inhibition of Carbonic Anhydrase Reduces Brain Injury After Intracerebral Hemorrhage
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Inhibition of Carbonic Anhydrase Reduces Brain Injury After Intracerebral Hemorrhage

机译：抑制碳酸酐酶减少脑出血后的脑损伤

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摘要

Carbonic anhydrase 1 (CA-1) is a metalloenzyme present at high concentrations in erythrocytes. Our previous studies showed that erythrocyte lysis contributes to brain edema formation after intracerebral hemorrhage (ICH), and a recent study indicates that CA-1 can cause blood–brain barrier disruption. The present study investigated the role of CA-1 in ICH-induced brain injury. There were three groups in the study. In the first, adult male Sprague Dawley rats received 100 μl autologous blood injection into the right caudate. Sham rats had a needle insertion. Rat brains were used for brain CA-1 level determination. In the second group, rats received an intracaudate injection of either 50 μl CA-1 (1 μg/μl) or saline. Brain water content, microglia activation, and neuronal death (Fluoro-Jade C staining) were examined 24 h later. In the third group, acetazolamide (AZA, 5 μl, 1 mM), an inhibitor of carbonic anhydrases, or vehicle was co-injected with 100 μl blood. Brain water content, neuronal death, and behavioral deficits were measured. We found that CA-I levels were elevated in the ipsilateral basal ganglia at 24 h after ICH. Intracaudate injection of CA-1 induced brain edema (79.0 ± 0.6 vs. 78.0 ± 0.2% in the saline group, p < 0.01), microglia activation, and neuronal death (p < 0.01) at 24 h. AZA, an inhibitor of CA, reduced ICH-induced brain water content (79.3 ± 0.7 vs. 81.0 ± 1.0% in the vehicle-treated group, p < 0.05), neuronal death, and improved functional outcome (p < 0.05). These results suggest that CA-1 from erythrocyte lysis contributes to brain injury after ICH.
机译：碳酸酐酶1（CA-1）是一种高浓度存在于红细胞中的金属酶。我们以前的研究表明，脑出血（ICH）后，红细胞溶解会促进脑水肿的形成，而最近的研究表明，CA-1可能导致血脑屏障破坏。本研究调查了CA-1在ICH引起的脑损伤中的作用。该研究分为三组。首先，成年雄性Sprague Dawley大鼠接受100μl自体血液注射到右尾状。假大鼠插入针头。大鼠大脑用于脑CA-1水平测定。在第二组中，大鼠接受尾状内注射50μlCA-1（1μg/μl）或生理盐水。 24小时后检查脑含水量，小胶质细胞活化和神经元死亡（Fluoro-Jade C染色）。在第三组中，将乙酰唑胺（AZA，5μl，1 mM），一种碳酸酐酶抑制剂或媒介物与100μl血液共注射。测量大脑的含水量，神经元死亡和行为缺陷。我们发现ICH后24小时，同侧基底神经节中CA-1水平升高。尾内注射CA-1会导致脑水肿（盐水组为79.0±0.6，盐水组为78.0±0.2％，p <0.01），小胶质细胞活化和24小时神经元死亡（p <0.01）。 CA的抑制剂AZA降低了ICH诱导的脑水含量（媒介物治疗组为79.3±0.7，而81.0±1.0％，p <0.05），神经元死亡和功能改善（p <0.05）。这些结果表明，来自红细胞溶解的CA-1有助于ICH后的脑损伤。

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  • 来源
    《Translational Stroke Research》 |2012年第1期|130-137|共8页
  • 作者

    Fuyou Guo; Ya Hua; Jinhu Wang; Richard F. Keep; Guohua Xi;

  • 作者单位

    R5018 Biomedical Science Research Building Department of Neurosurgery University of Michigan 109 Zina Pitcher Place Ann Arbor MI 48109-2200 USA;

    R5018 Biomedical Science Research Building Department of Neurosurgery University of Michigan 109 Zina Pitcher Place Ann Arbor MI 48109-2200 USA;

    R5018 Biomedical Science Research Building Department of Neurosurgery University of Michigan 109 Zina Pitcher Place Ann Arbor MI 48109-2200 USA;

    R5018 Biomedical Science Research Building Department of Neurosurgery University of Michigan 109 Zina Pitcher Place Ann Arbor MI 48109-2200 USA;

    R5018 Biomedical Science Research Building Department of Neurosurgery University of Michigan 109 Zina Pitcher Place Ann Arbor MI 48109-2200 USA;

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  • 正文语种 eng
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  • 关键词

    Acetazolamide; Brain edema; Carbonic anhydrase 1; Cerebral hemorrhage; Rats;

    机译：乙酰唑胺;脑水肿;碳酸酐酶1;脑出血;大鼠;

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