Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization
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 studie...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2021/9976912 |
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| author | Shaoxi Yan Mo Zhou Xiaoyun Zheng Yuanyuan Xing Juan Dong Mengwen Yan Rui Li |
| author_facet | Shaoxi Yan Mo Zhou Xiaoyun Zheng Yuanyuan Xing Juan Dong Mengwen Yan Rui Li |
| author_sort | Shaoxi Yan |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-5e3f7e97e592461dbf2e39d8f92e4331 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-5e3f7e97e592461dbf2e39d8f92e43312025-08-20T03:34:32ZengWileyMediators of Inflammation0962-93511466-18612021-01-01202110.1155/2021/99769129976912Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage PolarizationShaoxi Yan0Mo Zhou1Xiaoyun Zheng2Yuanyuan Xing3Juan Dong4Mengwen Yan5Rui Li6Department of Health Care, China-Japan Friendship Hospital, Ministry of Health, ChinaDepartment of Health Care, China-Japan Friendship Hospital, Ministry of Health, ChinaDepartment of Health Care, China-Japan Friendship Hospital, Ministry of Health, ChinaDepartment of Health Care, China-Japan Friendship Hospital, Ministry of Health, ChinaDepartment of Health Care, China-Japan Friendship Hospital, Ministry of Health, ChinaDepartment of Cardiology, China-Japan Friendship Hospital, ChinaDepartment of Health Care, China-Japan Friendship Hospital, Ministry of Health, ChinaInflammation 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.http://dx.doi.org/10.1155/2021/9976912 |
| spellingShingle | Shaoxi Yan Mo Zhou Xiaoyun Zheng Yuanyuan Xing Juan Dong Mengwen Yan Rui Li Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization Mediators of Inflammation |
| title | Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization |
| title_full | Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization |
| title_fullStr | Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization |
| title_full_unstemmed | Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization |
| title_short | Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization |
| title_sort | anti inflammatory effect of curcumin on the mouse model of myocardial infarction through regulating macrophage polarization |
| url | http://dx.doi.org/10.1155/2021/9976912 |
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