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Updated: Sep 3, 2025
Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by Promoting Macrophage M2 Polarization
Mei Yang1,2,3, Jun Xiong4, Qiang Zou1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Background:
Macrophage polarization is an important regulatory mechanism of ventricular remodeling. Studies have shown that sinapic acid (SA) exerts an anti-inflammatory effect. However, the effect of SA on macrophages is still unclear.
Objectives:
The purpose of the study was to investigate the role of SA in macrophage polarization and ventricular remodeling after myocardial infarction (MI).
Methods:
An MI model was established by ligating the left coronary artery. The rats with MI were treated with SA for 1 or 4 weeks after MI. The effect of SA on bone marrow-derived macrophages (BMDMs) was also observed in vitro.
Results:
Cardiac systolic dysfunction was significantly improved after SA treatment. SA reduced MCP-1 and CCR2 expression and macrophage infiltration. SA decreased the levels of the inflammatory factors TNF-α, IL-1α, IL-1β, and iNOS and increased the levels of the M2 macrophage markers CD206, Arg-1, IL-10, Ym-1, Fizz-1, and TGF-β at 1 week after MI. SA significantly increased CD68+/CD206+ macrophage infiltration. Myocardial interstitial fibrosis and MMP-2 and MMP-9 levels were decreased, and the sympathetic nerve marker TH and nerve sprouting marker GAP43 were suppressed after SA treatment at 4 weeks after MI. The PPARγ level was notably upregulated after SA treatment. In vitro, SA also increased the expression of PPARγ mRNA in BMDMs and IL-4-treated BMDMs in a concentration-dependent manner. SA enhanced Arg1 and IL-10 expression in BMDMs, and the PPARγ antagonist GW9662 attenuated M2 macrophage marker expression.
Conclusions:
Our results demonstrated that SA attenuated structural and neural remodeling by promoting macrophage M2 polarization via PPARγ activation after MI.
Insights
Sinapic acid (SA) improves heart function after myocardial infarction by promoting M2 macrophage polarization. This process, mediated by PPARγ activation, reduces inflammation and structural remodeling.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- Macrophage polarization critically regulates ventricular remodeling post-myocardial infarction (MI).
- Sinapic acid (SA) exhibits anti-inflammatory properties, but its role in macrophage polarization remains unclear.
Purpose of the Study:
- To investigate the effects of SA on macrophage polarization.
- To determine SA's impact on ventricular remodeling following MI.
Main Methods:
- Myocardial infarction (MI) model induced by coronary artery ligation in rats.
- SA treatment administered 1 or 4 weeks post-MI; in vitro studies on bone marrow-derived macrophages (BMDMs).
Main Results:
- SA treatment improved cardiac systolic function, reduced inflammatory markers (TNF-α, IL-1β), and decreased macrophage infiltration.
- SA promoted M2 macrophage polarization (increased CD206, Arg-1, IL-10) via PPARγ upregulation.
- SA attenuated myocardial fibrosis, MMP levels, and suppressed neural remodeling markers.
Conclusions:
- SA attenuates structural and neural remodeling after MI.
- SA promotes M2 macrophage polarization through PPARγ activation, offering therapeutic potential.
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