ABSTRACT
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.