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.

中文翻译：

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姜黄素通过调节巨噬细胞极化对小鼠心肌梗死模型的抗炎作用

炎症在心肌梗死（MI）后引起组织损伤并促进心室重构，而巨噬细胞的浸润和极化在调节MI后炎症中起重要作用。在这里，我们研究了姜黄素在心肌梗死后的抗炎功能，并研究了它与巨噬细胞极化的关系。在体内，姜黄素不仅在 MI 后 3 个月减弱心室重构，而且在 MI 后的前 7 天抑制炎症。重要的是，qPCR 和免疫化学的结果表明，姜黄素降低了 MI 后前 7 天 MI 小鼠心肌中 M1（iNOS、CCL2 和 CD86）的表达，但增加了 M2 巨噬细胞（Arg1、CD163 和 CD206）标志物的表达。流式细胞术分析表明姜黄素抑制 M1（CD45+Gr-1-CD11b+iNOS+ 细胞）但增强 M2 巨噬细胞（CD45+Gr-1-CD11b+Arg+ 细胞）在 MI 小鼠心肌中的扩张，在后 7 天内-MI。在体外，姜黄素降低 LPS/IFNγ-升高的 M1 巨噬细胞标志物（iNOS 和 CD86）表达和 M1 巨噬细胞（iNOS+F4/80+ 细胞）的比例，但增加 LPS/IFN γ -抑制 M2 巨噬细胞标志物（Arg1 和 CD206）的表达和 M2 巨噬细胞的比例（Arg1+F4/80+ 细胞）。此外，姜黄素部分通过 AMPK 调节 M1/M2 巨噬细胞极化。总之，姜黄素通过部分通过 AMPK 通路调节巨噬细胞极化来抑制 MI 诱导的炎症。