Effect of hyperbaric oxygen on cytochrome C, Bcl-2 and Bax expression after experimental traumatic brain injury in rats.
- Author:
Zhan LIU
1
;
Qing-fang JIAO
;
Chao YOU
;
Yan-jun CHE
;
Fang-zhong SU
Author Information
- Publication Type:Journal Article
- MeSH: Analysis of Variance; Animals; Apoptosis; physiology; Brain Injuries; pathology; therapy; Cytochromes c; biosynthesis; Disease Models, Animal; Hyperbaric Oxygenation; Immunohistochemistry; Male; Proto-Oncogene Proteins c-bcl-2; biosynthesis; Rats; Rats, Sprague-Dawley; bcl-2-Associated X Protein; biosynthesis
- From: Chinese Journal of Traumatology 2006;9(3):168-174
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo explore the effects of hyperbaric oxygen (HBO) treatment on the neuronal apoptosis at an earlier stage and the expressions of Cytochrome C (Cyt C), Bcl-2 (B-cell lymphoma-2 family) and Bax (Bcl-2 associated X protein) in rat brain tissues after traumatic brain injury (TBI).
METHODSForty adult rats were divided into two groups, i.e., Group A (the rats with untreated TBI) and Group B (rats with HBO treatment after TBI). Sections of brain tissues of these two groups were then detected at 3, 6, 12, 24, 72 hours after TBI by immunohistochemistry and electronmicroscope, respectively.
RESULTSHBO treatment could up-regulate the expression of Bcl-2 within 72 hours, reduce the release of Cyt C from mitochondria, attenuate the formation of dimeric Bax and alleviate the mitochondrial edema within 24 hours after TBI.
CONCLUSIONSHBO treatment can alleviate neuronal apoptosis after TBI by reducing the release of Cyt C and the dimers of Bax and up-regulating the expression of Bcl-2.
