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Updated: Jul 13, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression
Kwok-Tung Lu1, Chang-Yen Wu, Hao-Han Yen
1Department of Life Science, National Taiwan Normal University, Taipei, Taiwan.
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-1beta brain edema and neuronal damage were determined in these animals after TBI.
Results:
We found that both mRNA and protein of IL-1beta 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-1beta overexpression. The present study suggests that administration of bumetanide could significantly decreased TBI-induced inflammatory response and neuronal damage.
