Key result
Vaccarin improves post-MI cardiac function and reduces fibrosis in mice by suppressing NLRP3-mediated pyroptosis.
Why the study?
Does vaccarin ameliorate post-myocardial infarction ventricular remodeling and cardiac fibrosis in preclinical models?
Does vaccarin ameliorate post-myocardial infarction ventricular remodeling and cardiac fibrosis in preclinical models?
Preclinical evidence indicates that vaccarin attenuates post-MI ventricular remodeling and fibrosis by targeting NLRP3 inflammasome-mediated pyroptosis.
Hypothesis-generating for vaccarin in post-MI remodeling; human trials needed before clinical consideration.
BACKGROUND: Acute myocardial infarction (AMI) is currently one of the major causes of human mortality. In recent years, with the application and popularization of reperfusion therapies such as thrombolysis and coronary intervention, the mortality rate of AMI has been significantly reduced. However, the incidence and mortality of heart failure have shown an upward trend. Ventricular remodeling (VR) serves as the primary mechanism for the occurrence of heart failure after MI. METHODS: Vaccarin (VAC) is an effective monomeric component extracted from the seeds of Vaccaria segetalis, a traditional Chinese medicinal material. The aim of our study is to uncover the therapeutic effects of VAC on VR after MI through network pharmacology and in vivo/vitro experiments, and to explore its possible molecular mechanisms. RESULTS: The protein-protein interaction (PPI) network identified NLRP3 as a core target. Enrichment analysis demonstrated that the intersecting genes were enriched in the NOD-like receptor signaling pathway. Molecular docking results revealed a high binding affinity between VAC and NLRP3. In vivo and in vitro experiments verified that VAC significantly improved cardiac function, alleviated myocardial fibrosis in mice with MI, relieved hypoxia-induced cardiomyocyte injury, and enhanced cell viability. Additionally, VAC inhibited the TNF-α-mediated activation, migration and collagen synthesis of cardiac fibroblasts. It exerts therapeutic effects mainly by suppressing the NLRP3 inflammasome-mediated pyroptosis signaling pathway. CONCLUSION: VAC ameliorates post-MI VR via suppressing NLRP3 inflammasome-mediated cardiomyocyte pyroptosis and mitigating myocardial fibrosis.
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Yan et al. (2026) studied Post-myocardial infarction ventricular remodeling. Vaccarin was evaluated on Ventricular remodeling, cardiac function, myocardial fibrosis, and NLRP3 inflammasome-mediated pyroptosis. Vaccarin improved cardiac function and alleviated myocardial fibrosis in mice post-MI by suppressing NLRP3 inflammasome-mediated pyroptosis.
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