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目的研究缺血性脑卒中大鼠缺血周边脑组织的经典Wnt信号通路活性及干预该通路活性对缺血周边血管新生的影响。方法随机将50只雄性Wistar大鼠分为4组:假手术组(Sham组,n=10),脑缺血对照组(MCAO组,n=20),氯化锂干预组(Li Cl组,n=10),DKK1干预组(DKK1组,n=10)。免疫印迹法检测经典Wnt信号通路成分,FITC-dextran检测血管密度,多普勒血流仪检测血流量。结果脑缺血1 d后,与Sham组相比,MCAO组缺血周边脑组织细胞核蛋白及细胞浆蛋白中β-catenin表达水平显著下降(P<0.05),7 d时明显恢复,14 d时接近正常水平。与MCAO组相比,Li Cl组β-catenin表达水平及p-GSK-3β/GSK-3β比值提高(P<0.05),并且缺血周边血管密度及血流量增加(P<0.05);DKK1组变化相反,β-catenin表达水平及p-GSK-3β/GSK-3β比值降低(P<0.05),血管密度及血流量下降(P<0.05)。结论经典Wnt信号通路参与调节缺血性脑卒中后缺血周边的血管新生。
Objective To investigate the effects of canonical Wnt signaling pathway activity on ischemic peripheral brain tissue in ischemic stroke rats and intervention of this pathway on ischemic peripheral angiogenesis. Methods Fifty male Wistar rats were randomly divided into 4 groups: Sham operation group (n = 10), cerebral ischemia control group (n = 20), lithium chloride intervention group n = 10), DKK1 intervention group (DKK1 group, n = 10). Western blotting was used to detect the components of canonical Wnt signaling pathway. FITC-dextran was used to detect the vascular density and Doppler flowmetry was used to detect the blood flow. Results Compared with Sham group, the expression of β-catenin in nucleus and cytoplasm of ischemic brain tissue in MCAO group decreased significantly (P <0.05) at 1 d after cerebral ischemia, and recovered significantly at 7 d. At 14 d Close to normal level. Compared with MCAO group, the expression of β-catenin and the ratio of p-GSK-3β / GSK-3β in LiCl group increased (P <0.05), and the peripheral blood vessel density and blood flow increased In contrast, the expression of β-catenin and the ratio of p-GSK-3β / GSK-3β decreased (P <0.05), while the blood vessel density and blood flow decreased (P <0.05). Conclusion The canonical Wnt signaling pathway is involved in the regulation of angiogenesis in peripheral ischemic stroke after ischemic stroke.