ArticleOpen veterinary journal2026
Glycocalyx disruption mediates HP-PRRSV-induced microvascular endothelial dysfunction and underlies astragalus polysaccharide's antiviral efficacy.
Article in Open veterinary journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Article
- Antiviral Activity of Baicalin Against PRRSV In Vitro and in Infected Piglets.Veterinary sciences · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pulmonary microvascular endothelial cells (MVECs) are not only targets of the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) but also the pivotal hub of inflammation, interacting with alveolar macrophages to amplify the inflammatory response and determine the extent of tissue damage. Glycocalyx disruption in MVECs is often the initiating factor of numerous functional disorders, and astragalus polysaccharide (APS) has been shown to improve glycocalyx integrity in MVECs. Aim: This study aimed to investigate the mediating role of glycocalyx disruption in HP-PRRSV-induced pulmonary microvascular endothelial dysfunction and the glycocalyx contribution to the anti-HP-PRRSV efficacy of APS. Methods: Results: HP-PRRSV infection reduced the expression of heparan sulfate proteoglycan 2 (HSPG-2), glypican-1, and syndecan-1 proteoglycans. It also lowered labeled Lens culinaris agglutinin, Datura stramonium agglutinin, and Phaseolus vulgaris agglutinin-E -reactive glycan ligand levels in porcine pulmonary MVECs. However, APS significantly alleviated this damage. Furthermore, its infection decreased TEER, increased HRP-SA permeability, elevated vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression, promoted neutrophil TEM, and impaired their bactericidal activity. APS markedly suppressed HP-PRRSV replication and restored these virus-induced impairments. Conversely, enzymatic glycocalyx removal with HPA III intensified microvascular endothelial injury and largely weakened the APS's restorative effect. Conclusion: Glycocalyx disruption is a critical pathogenic event that orchestrates pulmonary microvascular endothelial dysfunction during HP-PRRSV infection. More importantly, we delineated a novel mechanism by which APS exerts its therapeutic effects.
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