The Decrease on Na+, K+-ATPase Activity in the Cortex, but not in Hippocampus, is Reverted by Antioxidants in an Animal Model of Sepsis
The Decrease on Na+, K+-ATPase Activity in the Cortex, but not in Hippocampus, is Reverted by Antioxidants in an Animal Model of Sepsis
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DOI：
10.1007/s12035-012-8297-2
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发表时间：
2012-10-01
影响因子：
5.1
通讯作者：
Streck, Emilio Luiz
中科院分区：
文献类型：
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作者：
Jeremias, Isabela Casagrande;Scaini, Giselli;Streck, Emilio Luiz
在本研究中，我们研究了盲肠结扎穿孔（CLP）诱导的脓毒症是否改变了大鼠海马和大脑皮层的Na+，K +-ATP酶活性，mRNA表达和脑水肿，以及抗氧化剂（ATX）治疗是否阻止了脓毒症诱导的改变。对大鼠进行CLP，并将其分为三组：假手术组; CLP-大鼠进行CLP而不进行任何进一步治疗;以及ATX-CLP加施用N-乙酰半胱氨酸加去铁胺。CLP或假手术后多次（6、12和24）处死大鼠，分离海马和大脑皮质。脓毒症后24 h海马Na+，K +-ATP酶活性受到抑制，ATX治疗不能阻止这种抑制。脓毒症后6、12和24 h大脑皮层Na+，K +-ATP酶活性也受到抑制。海马和大脑皮层Na+，K +-ATP酶催化亚基mRNA水平在脓毒症后无明显变化。ATX治疗仅在大脑皮层中防止Na+，K +-ATP酶抑制。Na+，K +-ATP酶抑制与脑含水量增加无关。总之，本研究表明，CLP诱导的脓毒症抑制Na+，K +-ATP酶活性的机制依赖于氧化应激，但这是不相关的增加脑含水量。
In the present study, we investigated whether sepsis induced by cecal ligation and puncture (CLP) modifies Na+, K+-ATPase activity, mRNA expression, and cerebral edema in hippocampus and cerebral cortex of rats and if antioxidant (ATX) treatment prevented the alterations induced by sepsis. Rats were subjected to CLP and were divided into three groups: sham; CLP-rats were subjected to CLP without any further treatment; and ATX-CLP plus administration of N-acetylcysteine plus deferoxamine. Several times (6, 12, and 24) after CLP or sham operation, the rats were killed and hippocampus and cerebral cortex were isolated. Na+, K+-ATPase activity was inhibited in the hippocampus 24 h after sepsis, and ATX treatment was not able to prevent this inhibition. The Na+, K+-ATPase activity also was inhibited in cerebral cortex 6, 12, and 24 h after sepsis. No differences on Na+, K+-ATPase catalytic subunit mRNA levels were found in the hippocampus and cerebral cortex after sepsis. ATX treatment prevents Na+, K+-ATPase inhibition only in the cerebral cortex. Na+, K+-ATPase inhibition was not associated to increase brain water content. In conclusion, the present study demonstrated that sepsis induced by CLP inhibits Na+, K+-ATPase activity in a mechanism dependent on oxidative stress, but this is not associated to increase brain water content.