Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression

Kwok Tung Lu, Chang Yen Wu, Hao Han Yen, Jeng Hsiung F. Peng, Chi Ling Wang, Yi Ling Yang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)404-409
Number of pages6
JournalNeurological Research
Issue number4
Publication statusPublished - 2007 Jun


  • IL-1
  • Na -K -2Cl -cotransporter
  • Traumatic brain injury

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology


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