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A proteomic study of the effects of ramipril on post‐infarction left ventricular remodelling in the rabbit
Author(s) -
Chen ChingYi,
Lee BaiChin,
Hsu HsiuChing,
Lin HungJu,
Chao ChiaLun,
Lin YenHung,
Ho YiLwun,
Chen MingFong
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.06.001
Subject(s) - ramipril , medicine , glutathione peroxidase , ejection fraction , myocardial infarction , cardiology , heart failure , endocrinology , ventricular remodeling , downregulation and upregulation , infarction , superoxide dismutase , pharmacology , oxidative stress , chemistry , biochemistry , blood pressure , gene
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.