黄芪甲苷联合血管内皮生长因子转染内皮祖细胞对心肌梗死模型大鼠的保护作用  

The protective effect of astragaloside Ⅳ plus vascular endothelial growth factor transfected endothelial progenitor cells on myocardial infarction model rats

作　　者：李梦华[1] LI Menghua

机构地区：[1]南阳医学高等专科学校,河南南阳473061

出　　处：《中医临床研究》2022年第34期12-16,共5页Clinical Journal Of Chinese Medicine

基　　金：河南省高等学校重点科研项目(22B360012)。

摘　　要：为证实黄芪甲苷联合血管内皮生长因子(Vascular Endothelial Growth Factor,VEGF)转染内皮祖细胞(Endothelial Progenitor Cells,EPCs)对心肌梗死大鼠的保护作用,建立心肌缺血/再灌注损伤(Myocardial Ischemia Reperfusion Injury,MIRI)模型。观察不同组别大鼠心肌组织、血管分布等病理学变化,以及相关炎性细胞因子及其上游调控基因和信号转导蛋白的关系,结果表明:黄芪甲苷联合基因干细胞具有促血管新生作用,并能有效抑制炎性细胞因子肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)及其上游调控因子核转录因子-κB p65(Nuclear factor-κB p65,NF-κB p65)和信号转运蛋白Toll样受体4(Toll-like receptor 4,TLR4)的表达,减少心肌炎性反应。可见联合治疗对大鼠MIRI具有积极的保护作用。In order to confirm the protective effect of astragaloside Ⅳ plus VEGF transfected EPCs on myocardial infarction rats, the MIRI rat models were established. The pathological changes of myocardial tissue and blood vessel distribution of rats in different groups, as well as the relationship between related inflammatory cytokines and their upstream regulatory genes and signal transduction proteins were observed, and the results show that astragaloside Ⅳ plus gene stem cells can promote angiogenesis. In addition, the combination therapy can also effectively inhibit the expressions of inflammatory cytokine TNF-α and its upstream regulator NF-κB p65, and signal transporter TLR4, and decrease the myocardial inflammatory response. It is concluded that the combination therapy has a positive protective effect on myocardial ischemia/reperfusion injury in rats.

关 键 词：黄芪甲苷 血管内皮生长因子 血管内皮祖细胞 心肌梗死 

分 类 号：R542.22[医药卫生—心血管疾病]