Apoptosis-related protein expression in rabbits with blast brain injury following early hyperbaric oxygen therapy  被引量:1

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

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作  者:Shaonian Xu Jiachuan Liu Yongming Zhang Chunlin Wang Jinbiao Wang Yanyan Yang Jian Huo Wenjiang Sun 

机构地区:[1]Department of Neurosurgery,the 105 Hospital of Chinese PLA,Hefei 230031,Anhui Province,China

出  处:《Neural Regeneration Research》2012年第17期1318-1324,共7页中国神经再生研究(英文版)

基  金:supported by the Eleventh-Five Major Subject of Nanjing Military Area Command (Functional MRI of HBOT for acute severe traumatic brain injury),No.06Z19;the Military Medical Science and Technology Innovation Foundation in 2009 (Clinical study of CTP and NRS in traumatic SAH patients),No. 09Z009

摘  要: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.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.

关 键 词:hyperbaric oxygen craniocerebral injury CASPASE-3 cytochrome c BAX Bcl-2 neural regeneration 

分 类 号:Q255[生物学—细胞生物学] TU998.12[建筑科学—市政工程]

 

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