Effect of HPN on the expression of hypoxia-related proteins after cerebral is-chemia-reperfusion injury in rats
Objective To Explore the effect of HPN on the expression of hypoxia-related proteins in cerebral is-chemia-reperfusion injury in rats.Methods Sixty male SD rats were randomly divided into a sham-operated group,a model group,and HPN low-dose,medium-dose,and high-dose groups(100,150,200 mg/kg,respec-tively),with 12 rats in each group.The model group and the HPN administration group were constructed as a right middle cerebral artery occlusion/reperfusion(MCAO/R)model by using the modified Longa wire bolus method,and a sham-operated rat with the isolation of the right internal carotid artery only was used as a control.The subsequent experiments were carried out 24 hours after reperfusion:Neurological deficit symptom was scored;TTC staining was used to determine the volume of cerebral infarction;HE staining was used to observe the pathological changes in the semi-dark zone area of the brain regions of each group.Real-time quantitative PCR(Real-Time PCR)was used to detect the gene expression of hypoxia-associated proteins HIF-1α and VEGF in the cerebral cortex;Western blot detected the protein expression of hypoxia-associated proteins HIF-1α and VEGF in the cerebral cortex.Results Compared with the model group,the HPN administration group significant-ly improved neurological deficits(P<0.05),reduced the volume of cerebral infarction,and significantly re-duced the expression of HIF-1α and VEGF proteins and genes in the cerebral cortex(P<0.01),thus protec-ting against cerebral ischemia/reperfusion injury.Compared with the low-dose group of HPN,the cerebral cortex of the medium-and high-dose groups of HPN showed significantly increased HIF-1α and VEGF protein and gene expression(P<0.05).Conclusion HPN had a significant neuroprotective effect in cerebral ischemia-reperfu-sion injury model rats,and the neuroprotective effect was more obvious with the increase of HPN administration dose,which significantly regulated the expression of hypoxia-related proteins HIF-1α and VEGF.