Abstract
Inflammation causes tissue damage and promotes ventricular remodeling after myocardial infarction (MI), and the infiltration and polarization of macrophages play an important role in regulating inflammation post-MI. Here, we investigated the anti-inflammatory function of curcumin after MI and studied its relationship with macrophage polarization. In vivo, curcumin not only attenuated ventricular remodeling 3 months after MI but also suppressed inflammation during the first 7 days post-MI. Importantly, the results of qPCR and immunochemistry showed that curcumin decreased M1 (iNOS, CCL2, and CD86) but increased M2 macrophage (Arg1, CD163, and CD206) marker expression in the myocardium of MI mice during the first 7 days post-MI. And flow cytometry analysis indicated that curcumin suppressed M1 (CD45+Gr-1-CD11b+iNOS+ cells) but enhanced M2 macrophage (CD45+Gr-1-CD11b+Arg+ cells) expansion in the myocardium of MI mice during the first 7 days post-MI. In vitro, curcumin decreased LPS/IFNγ-elevated M1 macrophage marker (iNOS and CD86) expression and the proportion of M1 macrophages (iNOS+F4/80+ cells) but increased LPS/IFNγ-suppressed M2 macrophage marker (Arg1 and CD206) expression and the proportion of M2 macrophages (Arg1+F4/80+ cells). In addition, curcumin modulates M1/M2 macrophage polarization partly via AMPK. In conclusion, curcumin suppressed the MI-induced inflammation by modulating macrophage polarization partly via the AMPK pathway.
Highlights
Myocardial infarction (MI) is myocardial necrosis caused by acute and persistent ischemia and hypoxia of the coronary arteries, and about 1.5 million people in the United States suffer from MI each year, while China has 500,000 [1, 2]
We found that 3 months after MI, the survival rate of MI mice in the untreated group was 46.67% (7/15), while that of MI mice treated with curcumin was 60.00% (9/15), but there was no significant difference in the 3-month overall survival between the two groups (P > 0:05, Figure 1)
There was no significant difference in the infarct size and lateral cardiomyocyte width (Figure 1) of MI mice, while the posterior and septal cardiomyocyte width in MI mice without any treatment was significantly higher than that of MI mice treated with curcumin (Figure 1)
Summary
Myocardial infarction (MI) is myocardial necrosis caused by acute and persistent ischemia and hypoxia of the coronary arteries, and about 1.5 million people in the United States suffer from MI each year, while China has 500,000 [1, 2]. Myocardial inflammation caused by ischemia is the key to repair a damaged myocardium, but persistent inflammation is the main factor leading to myocardial remodeling and causing impaired cardiac function [4, 5]. M1 macrophages have been found to be an important component of ventricular remodeling, leading to Mediators of Inflammation dilation and impaired function of the left ventricle through proinflammatory effects [10, 11]. Many scholars have emphasized that attenuating inflammation induced the ventricular remodeling by regulating the polarization of macrophages after myocardial infarction
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