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European Journal of Heart Failure 2008 10(8):740-748; doi:10.1016/j.ejheart.2008.06.001
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© 2008 European Society of Cardiology

A proteomic study of the effects of ramipril on post-infarction left ventricular remodelling in the rabbit

Ching-Yi Chena, Bai-Chin Leeb, Hsiu-Ching Hsub, Hung-Ju Linb, Chia-Lun Chaob, Yen-Hung Linb, Yi-Lwun Hob and Ming-Fong Chenb,*

a Department of Animal Science and Technology, National Taiwan University 50 Lane 155, Sec. 3, Keelung Rd., Taipei, Taiwan
b Department of Internal Medicine, National Taiwan University Hospital 7 Chung-Shan S Rd, Taipei, Taiwan

* Corresponding author. Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei, Taiwan. Tel.: +886 2 2312 3456x5059; fax: +886 2 3322 3937. E-mail address: mfchen{at}ntu.edu.tw, austinr3{at}yahoo.com.tw (M.-F. Chen).


  Abstract

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.

Key Words: Rabbit • Myocardial infarction • Ramipril • Antioxidative defence • Coronary ligation

Received November 23, 2007; Revised March 20, 2008; Accepted June 4, 2008


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