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Evidence-Based Supplement Research
Evidence-Based Supplement Research

Anemarrhena asphodeloides Polysaccharide Exerts Antiviral Activity Against Porcine Epidemic Diarrhea Virus Targeting ROS/Caspase-3 Dependent Apoptosis.

  • 2026-01
  • Transboundary and emerging diseases 2026(1)
    • Long Yin
    • Xiaotong Wang
    • Jianbin Wang
    • Yue Zhang
    • Wei Zhang
    • Ping Yan
    • Jingting Yao
    • Luyao Jiang
    • Song Gao
    • Changchao Huan

Study Design

Methods
Investigated inhibitory effects of Anemarrhena asphodeloides polysaccharide on PEDV infection in vitro, using network pharmacology and bioinformatics analysis to study antiviral mechanism involving apoptosis and oxidative stress.
  • Animal Study
Porcine epidemic diarrhea (PED) is the severe infectious disease caused by the porcine epidemic diarrhea virus (PEDV), characterized by the onset of watery diarrhea. Anemarrhena asphodeloides polysaccharide, extracted from Anemarrhena asphodeloides, presents potential applications as immunostimulatory and anticancer agent in alternative therapies. However, its antiviral activity remains unreported. This study investigates the inhibitory effects of Anemarrhena asphodeloides polysaccharide on PEDV infection. The findings demonstrate, for the first time, that Anemarrhena asphodeloides polysaccharide can effectively inhibit PEDV infection in a dose-dependent manner. It does not impact PEDV release and deactivation. Through the network pharmacology and bioinformatics analysis, we focused on the antiviral mechanism of Anemarrhena asphodeloides polysaccharides in terms of apoptosis and oxidative stress. We revealed that Anemarrhena asphodeloides polysaccharide significantly decreases oxidative stress and caspase-3 dependent apoptosis in infected cells. Apoptosis inhibitor Ac-DEVD-CHO and ROS scavenger NAC disrupt PEDV infection, and NAC reduces caspase-3 dependent apoptosis. This study provides preliminary evidence of the anti-PEDV activity of Anemarrhena asphodeloides polysaccharide by targeting ROS/caspase-3 dependent apoptosis, establishing it as novel anti-PEDV agent.

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