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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Aging+Neurosci
2018 ; 10
(ä): 207
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20-HETE Inhibition by HET0016 Decreases the Blood-Brain Barrier Permeability and
Brain Edema After Traumatic Brain Injury
#MMPMID30061822
Lu L
; Wang M
; Wei X
; Li W
Front Aging Neurosci
2018[]; 10
(ä): 207
PMID30061822
show ga
Recent studies have implicated 20-HETE as a vasoconstrictive mediator in trauma,
the purpose of this study was to determine whether administration of HET0016, the
20-HETE inhibitor, could protect neurons from trauma and the effect of HET0016 on
the blood-brain barrier (BBB) and brain edema in experimental traumatic brain
injury (TBI). Rat models with TBI were established. Brain edema was measured
according to the wet and dry weight method at 3, 24, and 72 h after injury. The
BBB permeability was quantified by dynamic contrast-enhanced magnetic resonance
imaging (DCE-MRI). Superoxide production, the activity of superoxide dismutase
(SOD) and total antioxidative capability (T-AOC) in traumatic brain tissues were
also measured. Western blot analysis was used to analyze the expression of the
occludin, ZO-1, Matrix metalloproteinase-9 (MMP-9), and c-Jun N-terminal protein
kinase (JNK) pathways. At 24 and 72 h after administration of HET0016 following
TBI, the BBB permeability and brain edema decreased. The decrease in superoxide
production and the increase in the activity of SOD and T-AOC were measured in
this study. Western blot analysis showed that the expression of MMP-9 and JNK
pathways was suppressed, but the expression of ZO-1 and occludin was increased.
These results suggest that the administration of HET0016 could protect the BBB
function and decrease brain edema after experimental traumatic injury by
suppressing the expression of MMP-9 and activating the expression of tight
junction proteins via suppressing the JNK pathway and oxidative stress.
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