Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 99-105 |
| Number of pages | 7 |
| Journal | European Journal of Pharmacology |
| Volume | 548 |
| Issue number | 1-3 |
| DOIs | |
| Publication status | Published - 2006 Oct 24 |
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Keywords
- Brain edema
- Bumetanide
- Na-K-2Cl cotransporter
- Traumatic brain injury
ASJC Scopus subject areas
- Pharmacology
Cite this
Inhibition of the Na+-K+-2Cl--cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage. / Lu, Kwok-Tung; Wu, Chang Yen; Cheng, Nai Chi; Wo, Yu Yuan Peter; Yang, Jen Tsung; Yen, Hao Han; Yang, Yi Ling.
In: European Journal of Pharmacology, Vol. 548, No. 1-3, 24.10.2006, p. 99-105.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibition of the Na+-K+-2Cl--cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage
AU - Lu, Kwok-Tung
AU - Wu, Chang Yen
AU - Cheng, Nai Chi
AU - Wo, Yu Yuan Peter
AU - Yang, Jen Tsung
AU - Yen, Hao Han
AU - Yang, Yi Ling
PY - 2006/10/24
Y1 - 2006/10/24
N2 - 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.
AB - 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.
KW - Brain edema
KW - Bumetanide
KW - Na-K-2Cl cotransporter
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=33748714959&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33748714959&partnerID=8YFLogxK
U2 - 10.1016/j.ejphar.2006.07.048
DO - 10.1016/j.ejphar.2006.07.048
M3 - Article
C2 - 16962576
AN - SCOPUS:33748714959
VL - 548
SP - 99
EP - 105
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
SN - 0014-2999
IS - 1-3
ER -