构建股骨骨折合并脑损伤模型大鼠低氧诱导因子1α和核心结合因子α1的表达

摘要

BACKGROUND:The low oxygen environment after femoral fracture and cerebral trauma wil induce series of related cytokines expression, including hypoxia-inducible factor 1αand core binding factorα1, which play key roles in regulating bone healing. However, whether the accelerated bone healing is correlated with the expression of hypoxia-inducible factor 1αand core binding factorα1 is stil unknown. OBJECTIVE:To construct rat models of brain injury, to compare the expression level of hypoxia-inducible factor 1αand core binding factorα1 in femoral fracture combined with cerebral trauma rats and simple femoral fracture rats, and to assess the influence of cerebral trauma on bone healing. METHODS:Rats were randomly divided into blank group, simple femoral fracture group and femoral fracture combined with cerebral trauma group. At 1, 2, 3 and 5 weeks after modeling, rats were executed. Bone healing was evaluated using femoral fracture end X-ray score and hematoxylin and eosin staining at cal us tissues. Besides, the expression levels of hypoxia-inducible factor 1αand core binding factorα1 of three groups were determined with immunohistochemistry. RESULTS AND CONCLUSION:Bone healing in the femoral fracture combined with cerebral trauma group was better than that of simple femoral fracture group. There was significant difference in the expression level of hypoxia-inducible factor 1αand core binding factorα1 between the simple femoral fracture group and femoral fracture combined with cerebral trauma group (P<0.05). At the same time, the level of simple femoral fracture group and femoral fracture combined with cerebral trauma group was significantly higher than that of blank group, and that in femoral fracture combined with cerebral trauma group was significantly higher than that of simple femoral fracture group (P<0.05). Results verified that the expression levels of hypoxia-inducible factor 1αand core binding factorα1 of rats with femoral fracture combined with cerebral trauma were significantly high, which may be the major reason why the bone healing was accelerated after fracture combined with brain injury.%背景：骨折及脑损伤后造成的低氧环境导致一系列相关因子的表达，包括低氧诱导因子1α和核心结合因子α1，二者在骨折愈合中具有重要的调控作用。但骨折合并脑损伤后骨折愈合加速是否与低氧诱导因子1α和核心结合因子α1的表达相关还不十分清楚。　　目的：构建脑损伤大鼠模型，对低氧诱导因子1α和核心结合因子α1在大鼠股骨骨折合并脑损伤及单纯股骨骨折模型的骨折愈合过程中表达的对比，评价脑损伤对骨折愈合的影响。　　方法：将大鼠随机分为空白组、单纯股骨骨折组和股骨骨折合并脑损伤组。造模后1，2，3，5周处死动物，通过股骨骨折断端X射线评分及骨痂组织进行苏木精-伊红染色评价模型大鼠不同时间点骨折愈合情况，通过免疫组织化学检测，评价3组低氧诱导因子1α和核心结合因子α1的表达。　　结果与结论：股骨骨折合并脑损伤组的骨折愈合情况优于单纯股骨骨折组。单纯股骨骨折和股骨骨折合并脑损伤两组的组内1，2，3，5周低氧诱导因子1α和核心结合因子α1的表达比较，差异有显著性意义(P<0.05)；同一时间段组间比较，单纯股骨骨折组和股骨骨折合并脑损伤组均明显高于空白组，股骨骨折合并脑损伤组高于单纯股骨骨折组(P <0.05)。结果证实，骨折合并脑损伤模型大鼠低氧诱导因子1α和核心结合因子α1表达更为突出，这可能是骨折合并脑损伤后骨折愈合加速的重要原因。