缺氧预处理对颅脑损伤大鼠脑组织HIF-1α及其HO-1表达的影响  

Effect of hypoxia preconditioning on the changes of HIF-1α and HO-1 in the brain tissue in rats with traumatic brain injury

作　　者：张磊[1] 刘家传[1] 杨艳艳[1] 王金标[1] 张星[1] 王春琳[1] 周治民[1] 

机构地区：[1]解放军105医院神经外科,l合肥23003

出　　处：《中国微侵袭神经外科杂志》2014年第12期566-569,共4页Chinese Journal of Minimally Invasive Neurosurgery

基　　金：全军医学科技"十二五"科研项目(编号:CWS11J262);2009年南京军区医学科技创新重点课题(编号:09Z009)

摘　　要：目的探讨缺氧预处理对颅脑损伤大鼠脑组织缺氧诱导因子(HIF-1α)及血红素氧合酶-1(HO-1)表达的影响。方法 Sprague-Dawley大鼠102只,随机分为对照组(n=6)、创伤组(n=48)和预处理组(n=48)。创伤组按照改进的Feeney自由落体撞击法建立大鼠颅脑损伤模型,预处理组给予缺氧预处理后,同法造模。采用RT-PCR和Western blotting观察伤后1 h、4 h、8 h、12 h和1 d、3 d、7 d、14 d挫伤周围脑组织HIF-1α、HO-1表达变化。结果创伤组与对照组比较,HIF-1α和HO-1在伤后4 h、8 h、12 h和1、3 d表达上调(P<0.05)。预处理组与创伤组比较,HIF-1α和HO-1在伤后1 h逐渐上调,伤后4 h、8 h、12 h和1、3 d表达显著上调,直至伤后7 d(P<0.05)。结论缺氧预处理可增加颅脑损伤后挫伤区周围脑组织HIF-1α的表达,进而促进HO-1 m RNA及蛋白表达。其机制可能是缺氧预处理提高颅脑损伤对缺氧的适应性,减轻挫伤周围脑组织氧自由基对神经细胞伤害。Objective To observe the effect ofhypoxic preconditioning on expression ofhypoxia inducible factor-1α （HIF-1α） and heme oxygenase-1 （HO-1） in brain tissue of rat with traumatic brain injury. Methods One hundred and two SD rats were randomly divided into control group （n = 6）, traumatic brain injury group （TBI group, n = 48） and hypoxic preconditioning group before TBI （HPC group, n = 48）. The rat TBI model was established by adopting improved Feeney flee falling method. The rats of HPC group were placed in a hypobaric chamber for hypoxic preconditioning and TBI was caused by the same method. The changes of HIF-1α and HO-1 were detected in each group on the 1, 4, 8, 12 h and 1, 3, 7, 14 d after injury by RT-PCR and Western blotting. Results Compared with the control group, the expressions of HIF-1α and HO-1 in the TBI group significantly increased at 4, 8, 12 h and 1, 3 d （P〈 0.05）. Compared with TBI group, the expression levels of HIF-1α and HO-1 increased at 1 h in the HPC group, and increased significantly at 4, 8, 12 h and 1, 3 d, and maintained until 7 d after injury （P 〈 0.05）. Condusions Hypoxia preconditioning can increase HIF-1α expression in the brain tissue surrounding contusion area after TBI, and then promote the expression of HO-1 mRNA and protein, which may be due to that hypoxic preconditioning improve the adaptation of the brain tissues to hypoxia and reduce the damage fi＇om oxygen radicals to nerve cells in the brain tissues surrounding contusion area.

关 键 词：颅脑损伤 缺氧 脑 缺氧诱导因子-1Α 血红素氧合酶-1 大鼠 

分 类 号：R651.15[医药卫生—外科学]