ArticleVirology journal2025
Mechanism research of Punicalagin in treating representative strains of enterovirus A and B types based on systems pharmacology and experimental validation.
Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
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Authors and funding
14 authors.
Funding
Abstract
backgroundEnteroviruses (EVs), particularly types A (e.g., EV-A71) and B (e.g., CVB3), cause severe complications in vulnerable populations. Limited vaccines and no antivirals underscore the need for broad-spectrum therapies. Punicalagin, a natural anti-inflammatory compound, was investigated for its pan-enteroviral therapeutic potential.
objectiveTo evaluate punicalagin's efficacy and mechanisms against multiple EV serotypes via integrated systems pharmacology and experimental validation.
methodsNetwork pharmacology identified punicalagin's targets and pathways. In vitro antiviral activity was assessed in Vero/A549 cells infected with EV-A71/CVB3. Neonatal mice were intraperitoneally inoculated with these viruses to test in vivo efficacy. Molecular docking, apoptosis assays, and inflammatory factor analyses elucidated mechanisms.
resultsPunicalagin inhibited EV-A71 and CVB3 replication in vitro and improved survival in infected mice. Systems pharmacology linked its effects to anti-apoptotic and anti-inflammatory pathways. Molecular docking confirmed interactions with apoptosis/inflammation regulators (e.g., CASP3, TNF-α). Experimental validation demonstrated reduced viral-induced apoptosis and suppressed IL-6/TNF-α levels.
conclusionPunicalagin exhibits broad-spectrum anti-enteroviral activity through dual inhibition of apoptosis and inflammation, validated across in vitro, in vivo, and computational models. This study provides a systems-level framework for repurposing natural compounds against phylogenetically diverse EVs, addressing critical therapeutic gaps for high-risk populations.
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