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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
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