兔颅脑爆炸伤后早期行高压氧治疗对Cyt C、Bax、Bcl-2表达的影响

目的 研究早期高压氧治疗(HBOT)对兔颅脑爆炸伤后脑皮质细胞色素C(Cty C)、Bax、Bcl-2的影响.方法 新西兰大白兔150只随机分为正常对照组(n=10)、创伤组(n=70)、HBOT组(n=70).创伤组和HBOT组建立兔颅脑爆炸伤模型,正常对照组不行爆炸伤.伤后1、6、12、24 h和3、7、14d,采用免疫组化方法观察3组兔脑皮质中cyt C、Bax、Bcl-2 的表达情况.结果 与正常对照组比较,创伤组伤后1h即出现CytC表达上升,伤后12 h达高峰,伤后24 h开始下降,但维持较高水平:HBOT组CytC的表达在伤后早期较创伤组下降明显(均P＜0.05).与正常对照组比较,创伤组Bax和Bcl-2 的表达在伤后1、6、12、24 h和3d均明显上调(均P＜0.05)；HBOT组Bax的表达在伤后早期较创伤组降低(P＜0.05),Bcl-2的表达则明显上调(P＜0.05).结论 早期高压氧治疗对颅脑爆炸伤后的脑保护作用可能与抑制Bax表达,诱导Bcl-2表达上调从而阻止伤后早期线粒体释放Cyt C有关.

The effect of early hyperbaric oxygen therapy on expressions of Cyt C, Bax and Bcl-2 after explosive brain injury in rabbits

Objective To investigate the effect of early hyperbaric oxygen therapy （HBOT） on the expressions of cytochrome C （Cyt C）, Bax and Bcl-2 in the cerebral cortex of rabbits after explosive brain injury. Methods One hundred and fifty New Zealand rabbits were randomly divided into the normal control group （n=10）, injury group （n=70） and HBOT group （n=70）. Explosive brain injury model was established in the injury group and HBOT group. No explosive injury was given to normal control group. The expressions of Cyt C, Bax and Bcl-2 in the cerebral cortex were detected in 3 groups by immunohistochemistry 1, 6, 12, 24 h and 3, 7, 14 d after injury. Results Compared with the normal control group, the expression of Cyt C increased at 1 h, reached peak at 12 h, and then decreased at 24 h after injury but still remained higher in the injury group. In the early stage after injury, the expression of Cyt C in HBOT group was lower than that in the injury group （all P〈0.05）. The expressions of Bax and Bcl-2 in the injury group were higher than those in the normal control group 1, 6, 12, 24 h and 3 d after injury （all P〈0.05）. Compared with the injury group, the expression of Bax decreased and the expression of Bcl-2 increased in HBOT group in the early stage after injury （both P〈0.05）. Conclusion The early HBOT can increase the expression of Bcl-2 and decrease the expression of Bax, thereby preventing the release ofCyt C from mitochondria in the early stage after explosive brain injury and playing cerebral protective role.