TY - JOUR
T1 - Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression
AU - Lu, Kwok Tung
AU - Wu, Chang Yen
AU - Yen, Hao Han
AU - Peng, Jeng Hsiung F.
AU - Wang, Chi Ling
AU - Yang, Yi Ling
PY - 2007/6
Y1 - 2007/6
N2 - 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 stuay suggests that administration of bumetanide could significantly decreased TBI-induced inflammatory response and neuronal damage.
AB - 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 stuay suggests that administration of bumetanide could significantly decreased TBI-induced inflammatory response and neuronal damage.
KW - IL-1
KW - Na -K -2Cl -cotransporter
KW - Traumatic brain injury
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U2 - 10.1179/016164107X204738
DO - 10.1179/016164107X204738
M3 - Article
C2 - 17626737
AN - SCOPUS:34547608963
SN - 0161-6412
VL - 29
SP - 404
EP - 409
JO - Neurological Research
JF - Neurological Research
IS - 4
ER -