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Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression.

Author(s): Lu KT, Wu CY, Yen HH, Peng JH, Wang CL, Yang YL

Affiliation(s): Department of Life Science, National Taiwan Normal University, Taipei, Taiwan.

Publication date & source: 2007-06, Neurol Res., 29(4):404-9.

Publication type: Research Support, Non-U.S. Gov't

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.

Page last updated: 2007-10-18

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