Inhibition of the Na+-K+-2Cl--cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage

Kwok-Tung Lu, Chang Yen Wu, Nai Chi Cheng, Yu Yuan Peter Wo, Jen Tsung Yang, Hao Han Yen, Yi Ling Yang

研究成果: 雜誌貢獻文章

43 引文 斯高帕斯(Scopus)

摘要

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 monohydrate 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 mm3). Administration of the NKCC1 inhibitor bumetanide (15 mg/kg, I.V.) significantly attenuated the contusion volume (464.03 ±23.62 mm3) 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.

原文英語
頁(從 - 到)99-105
頁數7
期刊European Journal of Pharmacology
548
發行號1-3
DOIs
出版狀態已發佈 - 2006 十月 24

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ASJC Scopus subject areas

  • Pharmacology

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