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Lu, K.T. et al.

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

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 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.[1]

References

Inhibition of the Na(+)-K(+)-2Cl(-)-cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage. Lu, K.T., Wu, C.Y., Cheng, N.C., Wo, Y.Y., Yang, J.T., Yen, H.H., Yang, Y.L. Eur. J. Pharmacol. (2006) [Pubmed]

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