Early treatment with Resolvin E1 facilitates myocardial recovery from ischaemia in mice

Br J Pharmacol. 2018 Apr;175(8):1205-1216. doi: 10.1111/bph.14041. Epub 2017 Oct 22.

Abstract

Background and purpose: An appropriate inflammatory response is necessary for cardiac healing after acute myocardial infarction (MI). Resolvin E1 (RvE1) is an anti-inflammatory and pro-resolution lipid mediator derived from eicosapentaenoic acid. Here we have investigated the effects of RvE1 on the recovery of cardiac function after MI in mice.

Experimental approach: Acute MI was induced by surgical ligation of the left anterior descending artery in male C57BL/6 mice. RvE1 (5 ng·g-1 ·day-1 ; i.p.) was given to mice at different times following MI. Cardiac function was monitored by transthoracic echocardiography at days 3, 7 and 14 after MI. Effects of RvE1 on the migration of subpopulations of monocytes/macrophages (Mos/Mps, Ly6Chi and Ly6Clow ) were examined by flow cytometry and transwell assay.

Key results: RvE1 administration from days 1 to 7 post-MI improved cardiac function, whereas treatment from days 7 to 14 markedly inhibited recovery of cardiac function. Early treatment with RvE1 post-MI suppressed the infiltration of dominant Ly6Chi Mos/Mps and secretion of pro-inflammatory cytokines in injured hearts, which protected cardiomyocytes against apoptosis in the peri-infarct zones. Contrastingly, treatment with RvE1 1 week after MI decreased infiltration of Ly6Clow Mos/Mps and expression of pro-angiogenic factors in cardiac tissue, consequently reducing neovascularization in the peri-infarct zones. Additionally, RvE1 inhibited Mp migration by activating ChemR23 receptors.

Conclusion and implications: Treatment with RvE1 during the initial 7 days after MI facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, indicating that RvE1 may serve as an early therapeutic agent for acute MI.

Linked articles: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adoptive Transfer
  • Animals
  • Cell Movement / drug effects
  • Cells, Cultured
  • Coculture Techniques
  • Cytokines / genetics
  • Eicosapentaenoic Acid / analogs & derivatives*
  • Eicosapentaenoic Acid / pharmacology
  • Eicosapentaenoic Acid / therapeutic use
  • Fibroblasts / drug effects
  • Fibroblasts / physiology
  • Macrophages, Peritoneal / drug effects
  • Macrophages, Peritoneal / physiology
  • Male
  • Mice, Inbred C57BL
  • Monocytes / drug effects
  • Monocytes / physiology
  • Monocytes / transplantation
  • Myocardial Infarction / drug therapy*
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / pathology
  • Myocardium / metabolism
  • Myocardium / pathology

Substances

  • Cytokines
  • Eicosapentaenoic Acid
  • 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid

Grants and funding