ArticleDrug design, development and therapy2022
Ginsenoside Rd Promotes Cardiac Repair After Myocardial Infarction by Modulating Monocytes/Macrophages Subsets Conversion.
Article in Drug design, development and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Challenges and opportunities for ginseng-based medicines in treating cardiac fibrosis from mechanistic insights to clinical translation.Chinese herbal medicines · 2026Review
- Macrophages of the heart: Homeostasis and disease.Biomedical journal · 2026Review
- A tripartite therapeutic agent reprograms the myocardial infarction microenvironment.Materials today. Bio · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Two-dimensional cell membrane chromatography guided screening of myocardial protective compounds from Yindan Xinnaotong soft capsule.Chinese medicine · 2025Article
- Ginseng and ginsenosides on cardiovascular and pulmonary diseases; Pharmacological potentials for the coronavirus (COVID-19).Journal of ginseng research · 2024Review
- Protective effects of ginseng and ginsenosides in the development of osteoarthritis (Review).Experimental and therapeutic medicine · 2023Review
- Ginsenoside Rg1 Delays Chronological Aging in a Yeast Model via CDC19- and SDH2-Mediated Cellular Metabolism.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors.
Funding
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Abstract
Purpose: This study aimed to elucidate the potential molecular mechanisms by which GSRd improves cardiac inflammation and immune environment after MI. Materials and Methods: The potential target genes of GSRd were predicted using the STITCH database. In vivo, MI mice models were established by left anterior descending ligation and were divided into the sham group, MI + Vehicle group, and MI + GSRd group. DMSO, DMSO, and GSRd 50 μL/day were intraperitoneally injected, respectively. After 28 days, echocardiography, Masson staining, immunofluorescence staining, flow cytometry, RT-PCR, and Western blot were performed. Mice peritoneal macrophages were extracted in vitro, and Western blot was performed after GSRd and/or Akt inhibitor MK2206 intervention. Results: GSRd significantly improved mouse myocardial function, attenuated cardiac fibrosis, and inhibited inflammation and apoptosis in myocardial tissues after myocardial infarction. Meanwhile, GSRd increased non-classical Ly6C Conclusion: GSRd can enhance the transformation of Ly6C
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