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

G Liu, Q Liu, Y Shen, D Kong, Y Gong… - British Journal of …, 2018 - Wiley Online Library
G Liu, Q Liu, Y Shen, D Kong, Y Gong, B Tao, G Chen, S Guo, J Li, S Zuo, Y Yu, H Yin
British Journal of Pharmacology, 2018Wiley Online Library
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; ip) was given to mice at …
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
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