Therapeutic effects of hyperbaric oxygen in a rat model of endothelin-1-induced focal cerebral ischemia

Abstract It has been established that hyperbaric oxygen (HBO) treatment reduces brain edema, decreases infarct volume, contributes to neurological functional recovery and suppresses apoptosis in suture-induced focal cerebral ischemic animal models. In the present study, we evaluated the therapeutic...

Full description

Saved in:
Bibliographic Details
Published inBrain research Vol. 1153; pp. 204 - 213
Main Authors Huang, Zhen-Xing, Kang, Zhi-Min, Gu, Guo-Jun, Peng, Guang-Neng, Yun, Liu, Tao, Heng-Yi, Xu, Wei-Gang, Sun, Xue-Jun, Zhang, John H
Format Journal Article
LanguageEnglish
Published London Elsevier B.V 11.06.2007
Amsterdam Elsevier
New York, NY
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Abstract It has been established that hyperbaric oxygen (HBO) treatment reduces brain edema, decreases infarct volume, contributes to neurological functional recovery and suppresses apoptosis in suture-induced focal cerebral ischemic animal models. In the present study, we evaluated the therapeutic effect of HBO in an endothelin-1-induced focal cerebral ischemia in rats and explored the associated mechanisms of HBO-induced brain protection. One hundred twenty male Sprague–Dawley rats (280 to 320 g) were randomly assigned to sham, focal cerebral ischemia and focal cerebral ischemia treated with HBO groups. Brain water content, neurological function, morphology and molecular biological markers were assessed. HBO (100% O2 , 2.5 atmosphere absolute for 2 h) was initiated at 1 h after focal cerebral ischemia. Rats were killed at 24 h to harvest tissues for Western blot or for histology. In HBO-treated animals, an enhanced ratio of Bcl-2 and Bax and a reduced expression of hypoxia-inducible factor-1α (HIF-1α) in the hippocampus after focal cerebral ischemia were observed. These results indicate that HBO provides brain protection that is probably associated with the inhibition of HIF-1α and the elevation of Bcl-2.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2007.03.061