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.
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
