Apoptosis-related protein expression in rabbits with blast brain injury following early hyperbaric oxygen therapy

We treated detonator-explosion-induced craniocerebral injury in rabbits with hyperbaric oxygen 1 24 hours post-injury. Expression of the apoptosis-regulating protein cytochrome c, the pro-apoptotic protein Bax and the apoptosis marker caspase-3 in the tissues surrounding the area of injury was signi...

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Published inNeural regeneration research Vol. 7; no. 17; pp. 1318 - 1324
Main Authors Xu, Shaonian, Liu, Jiachuan, Zhang, Yongming, Wang, Chunlin, Wang, Jinbiao, Yang, Yanyan, Huo, Jian, Sun, Wenjiang
Format Journal Article
LanguageEnglish
Published India Medknow Publications & Media Pvt. Ltd 15.06.2012
Department of Neurosurgery, the 105 Hospital of Chinese PLA, Hefei 230031, Anhui Province, China
Medknow Publications & Media Pvt Ltd
Subjects
Apoptosis
Bcl-2
caspase-3
Cytochrome
Cytoplasm
Explosions
Hypoxia
Ischemia
Laboratory animals
Mitochondria
Oxygen therapy
Permeability
Protein expression
Rabbits
Research and Report: Peripheral Nerve Injury and Neural Regeneration
Signal transduction
Traumatic brain injury
早期
相关蛋白表达
细胞凋亡
细胞色素c
颅脑损伤
高压氧治疗
New Zealand
China
Bcl-2
neural regeneration
Bax
craniocerebral injury
hyperbaric oxygen
cytochrome c
caspase-3
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Summary:We treated detonator-explosion-induced craniocerebral injury in rabbits with hyperbaric oxygen 1 24 hours post-injury. Expression of the apoptosis-regulating protein cytochrome c, the pro-apoptotic protein Bax and the apoptosis marker caspase-3 in the tissues surrounding the area of injury was significantly reduced, while that of the anti-apoptotic protein Bcl-2 was significantly increased. Our findings indicate that the curative effects of early hyperbaric oxygen on cortical cell apoptosis is associated with suppression of cytochrome c release from mitochondria. This mechanism underlies the observed reduction in Bax expression and upregulation of Bcl-2 expression.
Bibliography:hyperbaric oxygen; craniocerebral injury; caspase-3; cytochrome c; Bax; Bcl-2; neural regeneration
We treated detonator-explosion-induced craniocerebral injury in rabbits with hyperbaric oxygen 1 24 hours post-injury. Expression of the apoptosis-regulating protein cytochrome c, the pro-apoptotic protein Bax and the apoptosis marker caspase-3 in the tissues surrounding the area of injury was significantly reduced, while that of the anti-apoptotic protein Bcl-2 was significantly increased. Our findings indicate that the curative effects of early hyperbaric oxygen on cortical cell apoptosis is associated with suppression of cytochrome c release from mitochondria. This mechanism underlies the observed reduction in Bax expression and upregulation of Bcl-2 expression.
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Author contributions: Shaonian Xu, Yanyan Yang, Jian Huo and Wenjiang Sun provided and integrated experimental data. Shaonian Xu, Jiachuan Liu, Yongming Zhang, Chunlin Wang and Jinbiao Wang conceived and designed the study. Shaonian Xu and Jiachuan Liu analyzed experimental data. Shaonian Xu wrote the manuscript and provided technical support. Jiachuan Liu was in charge of funds, revised the manuscript and guided the study.
Shaonian Xu, Master, Department of Neurosurgery, the 105 Hospital of Chinese PLA, Hefei 230031, Anhui Province, China
ISSN:1673-5374
1876-7958
DOI:10.3969/j.issn.1673-5374.2012.17.006