[The studies of GLUT1 expression and neuron apoptosis in neonatal hypoxic-ischemia brain damage rat model].

OBJECTIVE: To investigate the relationship between the expression of glucose transporter protein 1 and the apoptosis of neuron during hypoxic-ischemia brain damage in neonatal rats. METHODS: Total 120 10-day old SD rats were divided into normal group, sham control group and hypoxic-ischemia (HI) group. In HI group, hypoxic-ischemia brain damage (HIBD) were generated according to Rice-Vannucci method, brain tissues were harvested at 2, 8, 24, 48 and 72 h after HI. The brain samples were also collected at the same time points in normal group and sham control group. The pathological changes was observed by hematoxylin-eosin (HE) staining, the mRNA expression of glucose transporter 1 (GLUT1) was detected by reverse transcriptase-polymerase chain reaction (RT-PCR), the protein expressions of GLUT1 and cleaved caspase-3 (CC3) were detected by immunohistochemistry, the apoptosis of neuron was measured by TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining. RESULTS: HE staining showed that the degree of brain cell damage increased with time after HI, the loss of neuronal cells peaked at 48 h, while the cells in control group apperanted in an orderly and normal morphology. The mRNA and protein expressions of GLUT1 were increased after HI, which began to increase at 2 h, and reach the peak at 24 h. and the expression levels at each time points were statistically higher (P< 0.01) than those in control group. CC3 protein expression also began to increase at 2 h, peaked at 48 h after HI, which was higher than that of control group (P<0.01). The number of positive cells was significantly increased after HI,with a peak at 48 h. CONCLUSION: The mRNA and protein expression of GLUT1 in brain tissue increased significantly after hypoxic-ischemia, and the peak time was earlier than that of CC3 protein and cellular apoptosis. This suggests that GLUT1 expression upregulation may be a certain degree of inhibition on neuronal apoptosis.