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Updated: Jul 4, 2026
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
A proteomic study of the effects of ramipril on post-infarction left ventricular remodelling in the rabbit
Ching-Yi Chen1, Bai-Chin Lee, Hsiu-Ching Hsu
1Department of Animal Science and Technology, National Taiwan University, 50 Lane 155, Sec. 3, Keelung Rd., Taipei, Taiwan.
Objectives:
In this study, we used a proteomic approach to investigate the potential proteins regulated by ramipril in post-infarction left ventricular remodelling in the rabbit.
Methods And Results:
Myocardial infarction (MI) was induced in male New Zealand White rabbits (2.5-3 kg) by ligation of the left anterior descending coronary artery. Two months later, the rabbits were either left untreated (MI group) or were treated daily for one month with 0.1 mg/kg wt of ramipril (ramipril group), then sacrificed. One month of ramipril treatment resulted in a significant improvement in the LV ejection fraction (LVEF) and a decrease in hydroxyproline content. The protein profiles of LV tissue showed that ramipril caused upregulation of glutathione peroxidase, superoxide dismutase (SOD), and heart-type fatty acid binding-protein (h-FABP) and downregulation of HSP27 and cyclophilin A. Ramipril treatment caused an increase in catalase, glutathione peroxidase, and SOD activity in the LV tissue. Oxidized glutathione levels and the GSSG/GSH ratio in the heart tissue were lower in the ramipril group than in the MI group.
Conclusions:
Ramipril increased antioxidative protein expression and enzyme activity, which could partly explain the role of ramipril in attenuating LV remodelling. In addition, the present study identifies several potential protein targets which may help to explain the mechanism by which ramipril exerts its effect in post-infarction LV remodelling in the rabbit.
Insights
Ramipril treatment improved cardiac function and reduced adverse remodeling after myocardial infarction in rabbits. It upregulated key antioxidant proteins and enzymes, suggesting a protective mechanism against heart damage.
Area of Science:
- Cardiovascular Research
- Proteomics
- Pharmacology
Background:
- Left ventricular remodeling is a detrimental process following myocardial infarction.
- Understanding the molecular mechanisms of drug action is crucial for improving cardiovascular therapies.
Purpose of the Study:
- To investigate proteins regulated by ramipril during post-infarction left ventricular remodeling in a rabbit model.
- To elucidate the molecular targets of ramipril's cardioprotective effects.
Main Methods:
- Myocardial infarction induced in rabbits, followed by ramipril treatment or no treatment.
- Proteomic analysis of left ventricular tissue to identify protein expression changes.
- Assay of enzyme activities and levels of oxidative stress markers.
Main Results:
- Ramipril treatment improved left ventricular ejection fraction and reduced hydroxyproline content.
- Upregulation of antioxidant proteins (glutathione peroxidase, superoxide dismutase, h-FABP) and downregulation of HSP27 and cyclophilin A observed.
- Increased activity of catalase, glutathione peroxidase, and SOD; decreased oxidized glutathione levels and GSSG/GSH ratio.
Conclusions:
- Ramipril enhances antioxidative protein expression and enzyme activity, contributing to the attenuation of left ventricular remodeling.
- Identified potential protein targets provide insights into ramipril's mechanism of action in post-infarction cardiac remodeling.
