The role of bradykinin B(1) and B(2) receptors for secondary brain damage after traumatic brain injury in mice.

Details

Serval ID
serval:BIB_9BA14FDC2E91
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The role of bradykinin B(1) and B(2) receptors for secondary brain damage after traumatic brain injury in mice.
Journal
Journal of Cerebral Blood Flow and Metabolism
Author(s)
Trabold Raimund, Eroes Christian, Zweckberger Klaus, Relton Jane, Beck Heike, Nussberger Juerg, Mueller-Esterl Werner, Bader Michael, Whalley Eric, Plesnila Nikolaus
ISSN
1559-7016[electronic]
Publication state
Published
Issued date
2010
Volume
30
Number
1
Pages
130-139
Language
english
Abstract
Inflammatory mechanisms are known to contribute to the pathophysiology of traumatic brain injury (TBI). Since bradykinin is one of the first mediators activated during inflammation, we investigated the role of bradykinin and its receptors in posttraumatic secondary brain damage. We subjected wild-type (WT), B(1)-, and B(2)-receptor-knockout mice to controlled cortical impact (CCI) and analyzed tissue bradykinin as well as kinin receptor mRNA and protein expression up to 48 h thereafter. Brain edema, contusion volume, and functional outcome were assessed 24 h and 7 days after CCI. Tissue bradykinin was maximally increased 2 h after trauma (P<0.01 versus sham). Kinin B(1) receptor mRNA was upregulated up to four-fold 24 h after CCI. Immunohistochemistry showed that B(1) and B(2) receptors were expressed in the brain and were significantly upregulated in the traumatic penumbra 1 to 24 h after CCI. B(2)R(-/-) mice had significantly less brain edema (-51% versus WT, 24 h; P<0.001), smaller contusion volumes ( approximately 50% versus WT 24 h and 7 d after CCI; P<0.05), and better functional outcome 7 days after TBI as compared with WT mice (P<0.05). The present results show that bradykinin and its B(2) receptors play a causal role for brain edema formation and cell death after TBI.
Keywords
Traumatic Brain Injury, Brain Edema, Inflammation, Bradykinin, Kallikerin-Kinin System, Neuroptotection, Controlled Cortical Impact, Kallikrein-Kinin System, Middle Cerebral-Artery, Binding-Sites, LF 16-0687MS, Rat Model, Edema, Antagonist, Permeability, Mediator
Pubmed
Web of science
Create date
26/01/2010 14:57
Last modification date
20/08/2019 15:02
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