Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression

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-1β brain edema and neuronal damage were determined in these animals after TBI.

Results: We found that both mRNA and protein of IL-1β 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-1β overexpression. The present study suggests that administration of bumetanide could significantly decreased TBI-induced inflammatory response and neuronal damage.

Keywords:

• TRAUMATIC BRAIN INJURY
• NA+ -K+ -2CL- -COTRANSPORTER
• IL-1