Why the study?
The immunoprotective mechanisms of ginsenoside Rd against post-MI HF, particularly its regulatory effects on regulatory T cells and monocytes/macrophages, warranted investigation.
Does ginsenoside Rd improve cardiac systolic function, reduce myocardial fibrosis, and modulate the cardiac immune microenvironment in a mouse model of post-myocardial infarction heart failure?
Does ginsenoside Rd improve cardiac systolic function, reduce myocardial fibrosis, and modulate the cardiac immune microenvironment in a mouse model of post-myocardial infarction heart failure?
This preclinical study demonstrates that ginsenoside Rd ameliorates post-myocardial infarction heart failure and myocardial fibrosis in mice by expanding regulatory T cells, upregulating IL-10, and promoting STAT3-mediated anti-inflammatory macrophage polarization.
Ginsenoside Rd should not yet alter post-MI HF care; leaves open immunoprotective translation from mouse models to human trials.
Purpose: This study aims to investigate the immunoprotective mechanisms of GSRd, an active ingredient of Panax ginseng C.A. Mey ( P. ginseng C.A. Mey), against post-MI HF, with particular focus on its regulatory effects on regulatory T cells (Tregs) and Monocytes/macrophages (Mos/Ms). Materials and Methods: UPLC-MS/MS was used to identify GSRd. A mouse post-MI HF model was established by LAD ligation to observe GSRd-mediated changes in Tregs, IL-10 and Mos/Ms. Network pharmacology predicted GSRd core targets against post-MI HF. Single-cell virtual knockout evaluated target function, while protein-protein docking predicted IL-10-core target binding regions. In vitro, LPS-stimulated RAW264.7 macrophages were applied for inflammatory modeling, with exogenous IL-10 as positive control and Stattic for functional reverse validation of GSRd. Results: UPLC-MS/MS confirmed GSRd in P. ginseng C.A. Mey. GSRd ameliorated cardiac function and alleviated myocardial fibrosis in post-MI HF mice. Immunologically, GSRd facilitated the recruitment of Tregs in failing myocardium and peripheral circulation and elevated IL-10 expression. Furthermore, GSRd promoted the polarization of Mos/Ms toward anti-inflammatory Ly6C low phenotype (with upregulated CD206 and Arg1), suppressed pro-inflammatory Ly6C high polarization, and reduced the secretion of TNF-ppressed pro-inflammatory Ly6Cin post-MI HF mice. Immunologically, GSRd facilitated the recruitment of Tregs in failing myocardium and peripheral ci of STAT3 in cardiac monocytes/macrophages predicted that STAT3 acts as a critical regulator maintaining cardiac inflammatory balance and immune homeostasis. Protein-protein interaction analysis predicted the binding domains between IL-10 and STAT3; molecular docking predicted that ginsenoside Rd can stably bind to Foxp3, IL-10 and STAT3. In vitro experiments revealed that GSRd promotes STAT3 phosphorylation to induce RAW264.7 macrophage polarization toward an anti-inflammatory phenotype, and Stattic attenuates the protective effects of GSRd. Conclusion: The present study demonstrates that GSRd confers therapeutic benefits against post-MI HF via modulating the cardiac immune microenvironment. Keywords: ginsenoside Rd, Panax ginseng C.A. Mey, post-myocardial infarction heart failure, regulatory T cells, monocytes/macrophages
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Zhao et al. (2026) studied this question.
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