Inhibition of the Na+-K+-2Cl--cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage
Inhibition of the Na+-K+-2Cl--cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage
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DOI：
10.1016/j.ejphar.2006.07.048
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发表时间：
2006-10-24
影响因子：
5
通讯作者：
Yang, Yi-Ling
中科院分区：
文献类型：
--
作者：
Lu, Kwok-Tung;Wu, Chang-Yen;Yang, Yi-Ling
本研究旨在利用脑创伤动物模型，探讨Na+-K+-2Cl（-）-协同转运蛋白（NKCC 1）在脑创伤后脑水肿、脑挫伤和神经元死亡中的作用。挫伤体积通过2，3，5，氯化三苯基四唑单水合物染色来验证。RT-PCR检测NKCC 1 mRNA的表达，Western blot检测NKCC 1蛋白的表达。结果发现，脑外伤后2 h脉络丛顶膜NKCC 1 RNA和蛋白表达开始上调，8h达高峰，持续24 h。实验组大鼠表现出严重的脑水肿（含水量：81.45 +/- 0.32%，而假手术组为78.38 +/- 0.62%），脑外伤后8小时挫伤体积显著增加（864.14 +/- 28.07 mm（3））。将NKCC 1抑制剂布美他尼（15 mg/kg，I. V.）明显减轻脑挫伤体积（464.03 ± 23.62 mm（3））和脑水肿（含水量：79.12 ± 0.28%）。我们的研究表明，NKCC 1有助于创伤性脑损伤诱导的脑水肿和神经元损伤。(c)2006 Elsevier B. V.保留所有权利。
The present study was aimed to elucidate the possible role of Na+-K+-2Cl(-)-cotransporter (NKCC1) on traumatic brain injury-induced brain edema, cerebral contusion and neuronal death by using traumatic brain injury animal model. Contusion volume was verified by 2,3,5,triphenyltetrazolium chloride momohydrate staining. NKCC1 mRNA expression was detected by RT-PCR and the protein expression of NKCC1 was measured by Western blot. We found that the expression of NKCC1 RNA and protein were up-regulated in choroid plexus apical membrane from 2 h after traumatic brain injury, peaked at 8 h, and lasted for 24 h. Rats in the experimental group displayed severe brain edema (water content: 81.45 +/- 0.32% compared with 78.38 +/- 0.62% of sham group) and contusion volume significantly increased 8 h after traumatic brain injury (864.14 +/- 28.07 mm(3)). Administration of the NKCC1 inhibitor bumetanide (15 mg/kg, I.V.) significantly attenuated the contusion volume (464.03 +/- 23.62 mm(3)) and brain edema (water content: 79.12 +/- 0.28%) after traumatic brain injury. Our study demonstrates that NKCC1 contributes to traumatic brain injury-induced brain edema and neuronal damage. (c) 2006 Elsevier B.V. All rights reserved.