Influence of ginsenoside Rg1 on myocardial angiogenesis in rats after myocardial infarction
- VernacularTitle:人参皂苷Rg1对大鼠心肌梗死后心肌血管再生的影响
- Author:
Xiehui CHEN
;
Jinjie LIANG
;
Xinsun LIU
;
Yun XU
- Keywords:
Myocardial infarction;
Ginsenosides;
Vascular endothelial growth factors;
Rats
- From:
Chinese Journal of cardiovascular Rehabilitation Medicine
2017;26(3):245-250
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore influence of ginsenoside Rg1 on coronary artery angiogenesis in rats with acute myocardial infarction (AMI) and its mechanism.Methods: A total of 120 Wistar rats were randomly and equally divided into sham operation group (only received thoracotomy to expose heart without coronary ligation),AMI group (no treatment after model development with ligating left coronary artery) and ginsenoside group (received ginsenoside Rg1 injection on 3h after AMI model development).Infarct area, expressions of vascular endothelial growth factor (VEGF) and its receptor (Flk-1), and VIII factor expression were respectively measured on 24h, one week and five weeks after model development.Results: Compared with sham operation group after five weeks, there were significant rise in myocardial infarction area, number of new blood capillaries and expression levels of VEGF and its receptor Flk-1 in ginsenoside group and AMI group, P<0.05 or <0.01;compared with AMI group, there was significant reduction in myocardial infarction area [(51.31±9.67)% vs.(29.33±6.70)%], and significant rise in number of new blood capillaries [(18.31±5.07) vs.(46.79±13.67)], expressions of VEGF [greyscale value: (84.3±8.7) vs.(32.9±16.7), greyscale value was inversely proportional to expression] and Flk-1 [(17.6±8.7) vs.(59.9±16.2)] in ginsenoside group, P<0.05 or <0.01.Conclusion: Application of ginsenoside Rg1 in AMI rat model can mobilize marrow stem cells gather in ischemic myocardium, upregulate expressions of VEGF and its receptor Flk-1, effectively promote angiogenesis of blood capillaries, and reduce myocardial infarction area.
