论文部分内容阅读
目的探讨新西兰兔脑组织局灶性缺血后再灌注实验动物模型的制作,研究局灶性脑缺血再灌注后新西兰兔脑组织缺氧诱导因子-1α的表达及意义。方法制备兔局灶性脑缺血3h再灌注6h、12h、1d、2d、3d、4d及对照组动物模型,通过免疫组化检测缺氧诱导因子-1(HIF-1)α蛋白的表达,RT-PCR检测HIF-1α基因表达的变化。结果免疫组化结果显示新西兰兔在缺血后再灌注6h开始,缺血侧脑组织梗死灶周边HIF-1α蛋白开始呈阳性表达,随再灌注时间的延长阳性表达进一步增强,一直持续到第3d,第4d开始下降;RT-PCR检测HIF-1α在6h后已有表达,随再灌注时间的延长,HIF-1α的表达呈上升的趋势,在第3d达高峰,第4d显著下降。结论脑缺血再灌注损伤可以诱导HIF-1α表达增强,提示HIF-1α对缺血性脑损伤有神经保护作用。
Objective To investigate the experimental animal model of focal ischemia-reperfusion in the brain of New Zealand rabbits and to study the expression and significance of hypoxia inducible factor-1α in the brain of New Zealand rabbits after focal cerebral ischemia-reperfusion. Methods The model of HIF-1α protein expression was detected by immunohistochemistry in the animal model of focal cerebral ischemia 3h after reperfusion for 6h, 12h, 1d, 2d, 3d, 4d. RT-PCR detection of HIF-1α gene expression changes. Results The results of immunohistochemistry showed that HIF-1αprotein began to be expressed around the infarct in ischemic brain tissue in New Zealand rabbits at 6h after reperfusion, and further increased with the reperfusion time until the 3rd day , And began to decline on the 4th day. The expression of HIF-1α was detected after 6 hours by RT-PCR. The expression of HIF-1α tended to increase with the prolongation of reperfusion time. Conclusions Cerebral ischemia-reperfusion injury can induce the expression of HIF-1α to be enhanced, suggesting that HIF-1α may have neuroprotective effects on ischemic brain injury.