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作 者:许少年[1] 刘家传[1] 王金标[1] 张永明[1] 杨艳艳[1] 霍健[1]
出 处:《中国微侵袭神经外科杂志》2012年第6期270-273,共4页Chinese Journal of Minimally Invasive Neurosurgery
基 金:南京军区十一五重点课题(编号:06Z19)
摘 要: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、14 d,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1 h即出现Cyt C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Cyt C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Bc1-2的表达在伤后1、6、12、24 h和3 d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),Bc1-2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Bc1-2表达上调从而阻止伤后早期线粒体释放Cyt C有关。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.
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