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Inhibition of carbonic anhydrase reduces brain injury after intracerebral hemorrhage

机译：抑制碳酸酐酶降低脑出血后的脑损伤

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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 hours 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 hours after ICH. Intracaudate injection of CA-1 induced brain edema (79.0 ± 0.6 vs. 78.0±0.2% in saline group, p<0.01)>, microglia activation and neuronal death (p<0.01) at 24 hours. 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）是在红细胞中以高浓度存在的金属酶。我们以前的研究表明，红细胞裂解在脑出血（ICH）之后有助于脑水肿形成，并且最近的研究表明CA-1可导致血脑屏障中断。本研究研究了Ca-1在ICH诱导的脑损伤中的作用。研究中有三组。首先，成年男性Sprague-Dawley大鼠接受了100μl自体血液注射到右侧>尾部尾部。假大鼠有针插入。大鼠大脑用于脑Ca-1水平测定。在第二组中，大鼠接受了含有50μlCa-1（1μg/μl）或盐水的粒化物注射。 24小时后检查脑水含量<强>，小胶鸡活化和神经元死亡（氟 - 玉染色）。在第三组中，乙酰唑胺（AZA，5μL，1mM），碳酸酐酶的抑制剂或载体被共注入100μL血液。测量脑含水量，神经元死亡和行为缺陷。我们发现在ICH后24小时内在同侧基础神经节升高了Ca-i水平。 Intracaudate注射Ca-1诱导的脑水肿（盐碱组79.0±0.6 vs.78.0±0.2％，P <0.01）<强>，微胶质增长 24小时，微胶质增生（P <0.01）。 AZA，Ca的抑制剂，降低ICH诱导的脑含水量（载体治疗组的79.3±0.7与81.0±1.0％，P <0.05），神经元死亡和改善功能结果（P <0.05）。结果建议从红细胞裂解中的Ca-1有助于ICH后的脑损伤。

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