摘要
目的研究缺氧预处理对创伤性颅脑损伤大鼠脑组织抗氧化应激和神经功能的影响。方法SD雄性大鼠48只采用随机数字表法分为假手术组、缺氧预处理组、颅脑损伤组、缺氧预处理＋颅脑损伤组，每组12只。采用低压氧舱预处理3d（-50kPa、3h／d）进行缺氧预处理，用改良的Feeney’s自由落体法制作颅脑损伤模型，伤后24h用改良的神经功能评分（mNSS）观察大鼠神经功能；免疫组化染色神经元核抗原（NeuN）检测神经元的存活：Western blotting和实时荧光定量PCR分别检测脑组织核转录因子NF-E2相关因子2（Nri2）、线粒体硫氧还蛋白还原酶2（TrxR2）蛋白和mRNA的表达。结果与假手术组、缺氧预处理组比较，颅脑损伤组、缺氧预处理＋颅脑损伤组大鼠mNSS评分增高，NeuN表达降低（0．274±0．033、0．281±0．042vs0．124±0．014、0．150±0．019），Nrf2、TrxR2蛋白和mRNA表达增高；与颅脑损伤组比较，缺氧预处理＋颅脑损伤组大鼠mNSS评分降低，NeuN表达增高，Nrf2、TrxR2蛋白和mRNA表达增高，差异均有统计学意义（P〈0．05）。结论缺氧预处理可增加颅脑损伤后脑组织抗氧化应激的水平，并减轻神经功能缺损。
Objective To research the influence of hypoxic preconditioning in anti-oxidative ability of brain tissues and neurological functions in rats after traumatic brain injury. Methods Forty eight adult male Sprague Dawley rats were randomly divided into sham-operated group, hypoxic preconditioning group （HPC）, traumatic brain injury group （TBI） and hypoxic preconditioning＋traumatic brain injury group （HPCT, n=12）. The HPC rat models were made by hypobaric chamber for 3 d （50 kPa, 3 h/d） and TBI were induced by Feeney＇s improved equipment. All rats were killed 24 h after injury, and the neurological functions of each group were evaluated by modified neurological severity scale （mNSS）; the neuronal survival around contusion area was detected by NeuN immunohistochemical staining, and the protein and mRNA expressions of nuclear transcription factor-related factor 2 （Nrt2） and thioredoxin reductases 2 （TrxR2） in the brain tissues were detected by Western blotting and real-time quantitative PCR. Results The mNSS scores in the TBI and HPCT groups were significantly higher as compared with those in the sham-operated and HPC groups （P〈0.05）, but those in the HPCT group was significantly lower than those in the TBI group （P〈0.05）. The neuronal survival in the TBI and HPCT groups was decreased as compared with that in the sham-operated and HPC groups （NeuN expressions： 0.274±0.033, 0.281±0.042 vs 0.124±0.014, 0.150±0.019）, with significant difference （P〈0.05）, while that in the HPCT group was statistically increased as compared with that in the TBI group （P〈0.05）. The expressions of Nrf2 and TrxR2 in the brain tissues of TBI and HPCT groups were significantly increased as compared with those in the sham-operated and HPC groups （P〈0.05）, and those in the HPCT group was significantly up-regnlated as compared with those in the TBI group （P〈0.05）. Conclusion HPC can increase the anti-oxidative ability and relieve the neurological functions missing after TB
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2014年第6期576-580,共5页
Chinese Journal of Neuromedicine
基金
全军医学科技“十二五”科研项目（CWS11J262）
2009年度南京军区医学科技创新重点课题（092009）
关键词
颅脑损伤
转录因子E2相关因子2
硫氧还蛋白还原酶2
缺氧预处理
Traumatic brain injury
Nuclear factor erythroid 2-related factor 2
Thioredoxinreductases 2
Hypoxic preconditioning
