Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect.

Abstract

Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial cardiac effects on chronic heart failure (CHF) recently. In this study, we attempted to investigate the mechanisms for the effect of ghrelin on ventricular remodeling following acute myocardial infarction (MI). Ligation of a coronary artery was used to create an MI in rats. One week after MI, ghrelin (100 microg/kg) or saline was injected subcutaneously twice a day for 4 weeks. When compared to sham groups, ghrelin administration significantly decreased left ventricular (LV) remodeling in post-MI rats, as indicated by increased LV maximum rate of pressure, LV fractional shortening and scar thickness; and decreased LV end-diastolic pressure, LV end-systolic diameter, LV end-diastolic diameter and cardiocytocytes apoptosis. Moreover, ghrelin inhibited the inflammatory response, as shown by decreased mRNA and protein levels of interleukin (IL)-1beta and tumor necrosis factor-alpha (TNF-alpha). Subsequently, the expression of matrix metalloproteinase (MMP)-2 and MMP-9 were also inhibited by ghrelin injection. Ghrelin alleviates LV dysfunction and ventricular remodeling in post-MI rats. This suggests that the beneficial effects of ghrelin on CHF may result from an inhibition of the inflammatory response.

• Authors: Cong-Xin Huang, Ming-Jie Yuan, He Huang, Gang Wu, Yu Liu, Sheng-Bo Yu, Hai-Tao Li, Tao Wang
• Journal: Peptides (Peptides) Vol. 30 Issue 12 Pg. 2286-91 (Dec 2009) ISSN: 1873-5169 [Electronic] United States
• PMID: 19747956 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents
• Ghrelin
• Interleukin-1beta
• Tumor Necrosis Factor-alpha
• Matrix Metalloproteinase 2
• Matrix Metalloproteinase 9

Topics

• Animals
• Anti-Inflammatory Agents (pharmacology)
• Blotting, Western
• Enzyme-Linked Immunosorbent Assay
• Ghrelin (pharmacology)
• In Situ Nick-End Labeling
• Interleukin-1beta (genetics, metabolism)
• Male
• Matrix Metalloproteinase 2 (genetics, metabolism)
• Matrix Metalloproteinase 9 (genetics, metabolism)
• Myocardial Infarction (immunology)
• Polymerase Chain Reaction
• Rats
• Rats, Sprague-Dawley
• Tumor Necrosis Factor-alpha (genetics, metabolism)
• Ventricular Remodeling (drug effects)