论文部分内容阅读
目的:探讨血管内皮生长因子(VEGF165)和血管生成素-1(angiopoietin-1)抑制心肌细胞凋亡的作用机制。方法:将编码人VEGF165或angiopoi-etin-1的复制缺陷型腺病毒载体(Ad-VEGF165或Ad-Ang1)转染大鼠心脏成肌细胞(H9C2),24h后以H2O2诱导细胞凋亡,分析VEGF165和an-giopoietin-1的抗凋亡作用。腺病毒转染24h后检测细胞中三磷酸肌醇激酶(phosphatidylinositol-3kinase)活性和bcl-2表达水平。结果:VEGF165和angiopoietin-1可不同程度抑制H9C2细胞凋亡。VEGF165和Ang1作用下细胞内三磷酸肌醇激酶活性和bcl-2表达水平增高。结论:VEGF165和/或Ang1可抑制心脏成肌细胞凋亡,这种保护作用与其激活细胞内三磷酸肌醇激酶途径和促进抗凋亡分子bcl-2的表达相关。血管生长因子VEGF165和angiopoietin-1的心脏成肌细胞保护作用为其功能学研究和临床应用开辟了新的方向。
Objective: To investigate the mechanism of vascular endothelial growth factor (VEGF165) and angiopoietin-1 inhibiting cardiomyocyte apoptosis. Methods: Human cardiac myoblast (H9C2) was transfected with replication-deficient adenoviral vector (Ad-VEGF165 or Ad-Ang1) encoding human VEGF165 or angiopoi-etin-1 and induced by H2O2 24 h later. Anti-apoptotic effects of VEGF165 and an-giopoietin-1. Apoptosis and phosphorylation of phosphatidylinositol-3 kinase (APK) and bcl-2 protein were detected 24h after transfection. Results: VEGF165 and angiopoietin-1 inhibited the apoptosis of H9C2 cells to varying degrees. Intracellular phosphoinositide kinase activity and bcl-2 expression were increased by VEGF165 and Ang1. CONCLUSION: VEGF165 and / or Ang1 can inhibit the apoptosis of cardiac myoblasts. This protective effect is related to the activation of intracellular phosphoinositide kinase pathway and the expression of anti-apoptotic molecule bcl-2. The cardiomyocyte protective effects of VEGF165 and angiopoietin-1 have opened up a new direction for their functional study and clinical application.