Background. After myocardial infarction, anti-inflammatory macrophages perform key homeostatic functions that facilitate cardiac recovery and remodeling. Several studies have shown that lactate may serve as a modifier that influences phenotype of macrophage. However, the therapeutic role of sodium lactate in myocardial infarction (MI) is unclear. Methods. MI was established by permanent ligation of the left anterior descending coronary artery followed by injection of saline or sodium lactate. Cardiac function was assessed by echocardiography. The cardiac fibrosis area was assessed by Masson trichrome staining. Macrophage phenotype was detected via qPCR, flow cytometry, and immunofluorescence. Signaling proteins were measured by Western blotting. Results. Sodium lactate treatment following MI improved cardiac performance, enhanced anti-inflammatory macrophage proportion, reduced cardiac myocytes apoptosis, and increased neovascularization. Flow-cytometric analysis results reported that sodium lactate repressed the number of the IL-6+, IL-12+, and TNF-α+ macrophages among LPS-stimulated bone marrow-derived macrophages (BMDMs) and increased the mRNA levels of Arg-1, YM1, TGF-β, and IL-10. Mechanistic studies revealed that sodium lactate enhanced the expression of P-STAT3. Furthermore, a STAT3 inhibitor eliminated sodium lactate-mediated promotion macrophage polarization. Conclusion. Sodium lactate facilitates anti-inflammatory M2 macrophage polarization and protects against MI by regulating P-STAT3.

中文翻译：

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乳酸钠加速 M2 巨噬细胞极化并改善小鼠心肌梗死后的心脏功能

背景。心肌梗塞后，抗炎巨噬细胞执行促进心脏恢复和重塑的关键稳态功能。多项研究表明，乳酸可作为影响巨噬细胞表型的修饰剂。然而，乳酸钠在心肌梗死（MI）中的治疗作用尚不清楚。方法。MI是通过永久结扎左冠状动脉前降支，然后注射盐水或乳酸钠来建立的。通过超声心动图评估心脏功能。通过马森三色染色评估心脏纤维化区域。通过 qPCR、流式细胞术和免疫荧光检测巨噬细胞表型。通过蛋白质印迹测量信号蛋白。结果. 心肌梗死后的乳酸钠治疗可改善心脏功能、增强抗炎巨噬细胞比例、减少心肌细胞凋亡和增加新血管形成。流式细胞仪分析结果显示，乳酸钠抑制LPS 刺激的骨髓源性巨噬细胞 (BMDM)中 IL-6+、IL-12+ 和 TNF- α + 巨噬细胞的数量，并增加 Arg- 的 mRNA 水平。 1、YM1、TGF- β和 IL-10。机理研究表明，乳酸钠可增强 P-STAT3 的表达。此外，STAT3 抑制剂消除了乳酸钠介导的促进巨噬细胞极化。结论。乳酸钠通过调节 P-STAT3 促进抗炎 M2 巨噬细胞极化并防止 MI。