ArticleIn vitro cellular & developmental biology. Animal2025
Ginsenoside Rg1 mitigates myocardial ischemia/reperfusion injury by inhibiting NLRP3-mediated pyroptosis.
Article in In vitro cellular & developmental biology. Animal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Ginsenoside Rc exerts protective effects against cerebral ischemia‒reperfusion injury by boosting the Nrf2 pathway through targeted activation of Sirt1.In vitro cellular & developmental biology. Animal · 2026Article
- Interfacial and Molecular Mechanisms of Pancreatic Lipase Modulation by Saponin-Rich Extracts with Antioxidant Activity.Molecules (Basel, Switzerland) · 2026Article
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4 authors.
Funding
Abstract
Nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and pyroptosis exert the pivotal influence on myocardial ischemia/reperfusion (I/R) injury. Ginsenoside Rg1 (Rg1) reportedly has multiple pharmacological actions. However, the cardioprotective potential and underlying mechanism of Rg1 in treating myocardial I/R injury in the context of pyroptosis have not been comprehensively investigated. A rat model of myocardial I/R injury was established by blocking the left anterior descending coronary artery for 30 min followed by reperfusion for 120 min. The prevention of Rg1 against I/R-caused damage and the potential mechanisms were explored. In our study, NLRP3 overexpression abolished the cardioprotective effect of Rg1, and Rg1 treatment improved myocardial function and changes in histological morphology and suppressed I/R-induced cytotoxicity as well as cardiomyocyte pyroptosis by reducing the pyroptosis-related proteins. These results indicate that Rg1 mitigated I/R-induced myocardial damage and pyroptosis by dramatically suppressing NLRP3 inflammasome activation and may provide new insights for the treatment of ischemic heart disease.
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Registered trials
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