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Am J Transl Res. 2019 Aug 15;11(8):5212-5226. eCollection 2019.

Resveratrol improves cardiac function by promoting M2-like polarization of macrophages in mice with myocardial infarction.

Author information

1
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University Nanjing, Jiangsu, P. R. China.
2
Department of Cardiology, The Affliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital Suzhou, Jiangsu, P. R. China.
3
Department of Ultrasound, The First Affiliated Hospital of Nanjing Medical University Nanjing, Jiangsu, P. R. China.
4
Atherosclerosis Research Center, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University Nanjing, Jiangsu, P. R. China.

Abstract

Macrophage polarization determines the transition from the inflammation phase to the inflammation resolution phase after myocardial infarction (MI). The aim of the present study was to investigate whether resveratrol (RSV) could inhibit the inflammatory mediators associated with the regulation of macrophage phenotypes and functions in MI mice. We initially discovered that RSV significantly improved cardiac function and suppressed the expression of fibrosis markers, such as collagen-I, collagen-III, and fibronectin, and pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α). RSV inhibited the expression of M1-like macrophage-related biomarkers (e.g., TNF-α and MCP-1) when bone marrow-derived macrophages (BMDMs) were stimulated with lipopolysaccharide (LPS) and interferon-γ (INF-γ). In contrast, it upregulated M2-like macrophage-related biomarkers (e.g., CD163 and Arg-1) when BMDMs were stimulated with interleukin-4 (IL-4) and interleukin-10 (IL-10). In addition, we found that RSV promoted M2-like macrophage polarization under anoxic conditions, which could be related to JAK2-SATA3 phosphorylation. In summary, RSV might promote anti-inflammatory M2-like polarization of macrophages after MI to improve cardiac function via the regulation of JAK2-SATA3 phosphorylation.

KEYWORDS:

JAK2-SATA3 phosphorylation; Resveratrol; inflammation; macrophage polarization; myocardial infarction

PMID:
31497235
PMCID:
PMC6731431

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