Effect Of Hyperglycemia On The Expression Of Glucose Transporter 1 And Glucose Transporter 3 In Rats Following Traumatic Brain Injury

Objective: To explore the effect of hyperglycemia on the expression of glucose transporter 1 and glucose transporter 3 in rats at the acute phase of traumatic brain injury.Methods: Adult male SD rats were randomly divided into 3 groups: normal control group, traumatic brain injury group and insulin treated group, the blood glucose concentration of the rats was measured before and after injury. The expression of GLUT-1 ,GLUT-3 gene and protein in the injured and uninjured cortex was detected by reverse transcription polymerase chain reaction (RT-PCR) and western-blot. The apoptosis of the injured and uninjured cortex were detected by TUNEL staining. The changes of neuronspecifienolase positive-Staining cells and single neuron neuronspecifienolase expression were examined by immunofluorescence .Longa, balance test and screen test score were used to assess neural functional defect.Results: The blood glucose concentration only increased markedly in traumatic brain injury group. Through the expression of GLUT-1 gene and protein decreased in the injured cortex both in the traumatic brain injury group and the insulin treated group, there was much more expression of GLUT-1 gene and protein at 12h, 24h, 48h, 72h after injury in the insulin treated group(P<0.05). Through the expression of GLUT-3 gene and protein increased in the injured cortex both in the traumatic brain injury group and the insulin treated group, there was much more expression of GLUT-3 gene and protein at 12h, 24h, 48h, 72h after injury in the insulin treated group(P<0.05).There were much more neuronspecifienolase positive- Staining cells and single neuron neuronspecifienolase expression but less apoptotic cells and neural functional defect in the insulin treated group. Meanwhile no changes were found in the uninjured cortex of each group(P>0.05).Conclusion: The hyperglycemia after traumatic brain injury might increase brain apoptosis and neural functional defect and decrease the neuronspecifienolase positive- Staining cells by decreasing the expression of GLUT-1 and GLUT-3.