Biological Significance Of Expression Changes IGF-I In Rats After Craniocerebral Injury Combined Fracture By Hypoxia

Insulin- like growth factorⅠ( IGF-Ⅰ) is a molecular similar to insulin polypeptide in the structure, mainly synthesized and secreted by the cells in the liver. Under normal physiological conditions, Growth Hormone(GH)- insulin-like growth factor-I axis(GH-IGF-I) is participate in the process of bone development.Increasing GH concentration mediates a longitudinal bone growth, through prompting IGF-I concentration of the circulatory system and local bone tissue, inducing the activation of vitamin D, and synthesizing sulfuric acid mucopolysaccharides collagen. When Craniocerebral injury combined fracture happened, in order to repair the damage of central nervous system cells,the body increased IGF-1 of circulatory system and bone’s local tissue area to stimulate periosteal bone formation contributing to accelerate fracture healing. Hypoxia can regulate the body’s IGF-I expression as an independent factor. Studies have shown that chronic hypoxia inhibits GH-IGF-I axis, suggesting that environmental hypoxia may not be conducive to fracture healing. In the clinical work, we have found out fracture healing accelerated after craniocerebral injury in plateau area.Therefore, IGF-I levels are influenced by hypoxia in high altitude? it will lead to fracture healing faster? This is a problem we think about. Accordingly, we have established Craniocerebral injury combined fractures and simple fractures of SD rat animal model, observing IGF-I expression in serum, local bone callus and fracture healing of SD rats with brain injury in chronic hypoxia. In this study, fracture healing assessed using imaging diagnostic methods, and IGF-I expression of serum and callus tissue detected appling the Elisa and immunohistochemical method. We discussed The basic mechanism which traumatic brain injury promoted fracture healing at high altitude hypoxic environment.The main achievement of this study is listed as follows:1. imaging diagnostic results revealed that fracture healing after brain injury was significantly better than the simple fracture, callus formation and transformation inadvance and fracture healing acceleration.2.Elisa assay showed that serum IGF-I of craniocerebral injury combined fracture of was significantly higher than other groups among different groups; serum IGF-I of simple brain damage in the second, higher than fracture group; serum IGF-I of control group,sham brain damage, sham brain damage merger was no significant difference. Comparing Serum IGF-I content of each group at 3,7,15,30 days different time points, it is found serum IGF-I content peak at 15 days among simple brain damage group, simple fracture group and craniocerebral injury combined fracture group. There were significant differences among 3,7,15,30 days different time points about serum IGF-I content, control group, sham brain damage, sham brain damage merger fracture group had no significant difference at different time points.3.using Immunohistochemistry localized callus IGF-I content, The results indicate the obvious increasing of local bone’s IGF-I expression between brain damage and craniocerebral injury combined fracture group.Conclusion:1. Comparative Analysis differences in fracture healing between simple fracture group and craniocerebral injury combined fracture group, founding that and brain injury promoting fracture healing is faster than simple fracture group.2.There are expression differences between serum IGF-I and local fracture’s IGF-I in among control group, sham-operated group of brain damage, brain damage and fracture differences sham, simple brain damage group, simple fracture group, craniocerebral injury combined fracture group, suggesting that IGF-I expression increased play an important positive role on bone healing in craniocerebral injury combined fracture group.In summary, chronic hypoxia can suppress GH-IGF-I axis in plateau, but IGF-I concentrations increased by craniocerebral injury combined fracture, more higher than the chronic hypoxia inhibition of GH-IGF-I axis. Therefore, undering chronic hypoxia condition, brain injury still promote healing acceleration by means of local bone callus and serum IGF-I expression.