Authors: Lu, Kwok-Tung¹; Wu, Chang-Yen²; Yen, Hao-Han²; Peng, Jeng-Hsiung²; Wang, Chi-Ling³; Yang, Yi-Ling²

Source: Neurological Research, Volume 29, Number 4, June 2007 , pp. 404-409(6)

Publisher: Maney Publishing

Abstract:

Objective: To examine the effects of administration of bumetanide, a specific NKCC1 inhibitor, on traumatic brain injury (TBI)-induced interleukin-1 (IL-1) expression.

Methods: TBI model was induced by the calibrated weight drop device (450 g in weight, 2.0 m in height) in adult rats based on procedures previously reported. One hundred and sixty Wistar rats were divided into sham-control group and experimental group for time course works of TBI. The expression of IL-1? brain edema and neuronal damage were determined in these animals after TBI.

Results: We found that both mRNA and protein of IL-1? were up-regulated in the hippocampus 3?24 hours after TBI. Animals displayed severe brain edema and neuron damage after TBI. Bumetanide (15 mg/kg), a specific Na⁺ ?K⁺ ?2Cl^? cotransporter inhibitor, significantly attenuated the TBI-induced neuronal damage by IL-1? overexpression. The present study suggests that administration of bumetanide could significantly decreased TBI-induced inflammatory response and neuronal damage.

Keywords: NA+ -K+ -2CL- -COTRANSPORTER; IL-1; TRAUMATIC BRAIN INJURY

Document Type: Research Article

DOI: http://dx.doi.org/10.1179/016164107X204738

Affiliations: 1: Department of Life Science, National Taiwan Normal University, Taipei, Taiwan 2: Institute of Biotechnology, National Chia-Yi University, Chia-Yi, Taiwan 3: General Education Center, National Chia-Yi University, Chia-Yi, Taiwan

Publication date: 2007-06-01

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