ArticleChinese medicine2024
Prunella vulgaris polysaccharide inhibits herpes simplex virus infection by blocking TLR-mediated NF-κB activation.
Article in Chinese medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- The cell-type-specific roles of Toll-like receptors in herpes simplex virus infection and pathogenesis.Virulence · 2026Review
- Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress.Molecular neurobiology · 2026Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- The immunomodulatory effects of sodium new houttuyfonate on different states of macrophage against Aspergillus fumigatus infection via distinct mechanism in invasive pulmonary aspergillosis.Chinese medicine · 2025Article
- Progress on the Anti-Inflammatory Activity and Structure-Efficacy Relationship of Polysaccharides from Medical and Edible Homologous Traditional Chinese Medicines.Molecules (Basel, Switzerland) · 2024Review
- Anti-HSV-1 agents: an update.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrunella vulgaris polysaccharide extracted by hot water and 30% ethanol precipitation (PVE30) was reported to possess potent antiviral effects against herpes simplex virus (HSV) infection. However, its anti-HSV mechanism has not yet been fully elucidated. PURPOSE: This study aimed to investigate the potential mechanisms of PVE30 against HSV infection.
methodsAntiviral activity was evaluated by a plaque reduction assay, and the EC
resultsThe P. vulgaris polysaccharide PVE30 was shown to compete with heparan sulfate for interaction with HSV surface glycoprotein B and gC, thus strongly inhibiting HSV attachment to cells. In addition, PVE30 downregulated the expression of IE genes, which subsequently downregulated the expression of E and L viral gene products, and thus effectively restricted the yield of progeny virus. Further investigation confirmed that PVE30 inhibited TLR2 and TLR3 signalling, leading to the effective suppression of NF-κB activation and IL-6 and TNF-α expression levels, and blocked HSV-1-induced necroptosis by reducing HSV-1-induced phosphorylation of MLKL.
conclusionOur results demonstrate that the P. vulgaris polysaccharide PVE30 is a potent anti-HSV agent that blocks TLR-mediated NF-κB activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.