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Total astragalosides decrease apoptosis and pyroptosis by inhibiting enterovirus 71 replication in gastric epithelial

Xiaoyan Zhang1, Jinfang Hao1, Chenxi Sun1

  • 1Department of Laboratory Medicine of Fenyang College, School of Pharmaceutical Science, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.

Experimental and Therapeutic Medicine
|February 28, 2022
PubMed
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This summary is machine-generated.

Total astragalosides (ASTs) from Astragalus membranaceus protect gastric cells from Enterovirus 71 (EV71) infection. ASTs reduce EV71-induced cell death, apoptosis, and pyroptosis, offering potential antiviral treatment.

Area of Science:

  • Virology
  • Immunology
  • Pharmacology

Background:

  • Enterovirus 71 (EV71) causes severe hand, foot, and mouth disease in children.
  • EV71 infection induces programmed cell death, with no specific antiviral drugs currently approved.
  • Astragalus membranaceus (AM), a Traditional Chinese medicine, has demonstrated antiviral properties.

Purpose of the Study:

  • To investigate the protective effects of total astragalosides (ASTs), bioactive components of AM, against EV71 infection.
  • To determine if ASTs can mitigate EV71-induced cell damage and programmed cell death in gastric epithelial cells.

Main Methods:

  • DAPI nuclear staining to observe nuclear morphology changes.
  • Cell Counting Kit-8 and lactate dehydrogenase (LDH) assays to assess cell viability and damage.
Keywords:
apoptosisenterovirus 71pyroptosisreplicationtotal astragaloside

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  • Western blotting and RT-qPCR to evaluate apoptosis, pyroptosis, and anti-EV71 activity.

    • Main Results:

    • EV71 infection caused nuclear shrinkage, decreased cell viability, and induced apoptosis and pyroptosis in GES-1 cells.
    • ASTs reversed EV71-induced nuclear shrinkage and protected GES-1 cells from apoptosis and pyroptosis.
    • ASTs demonstrated anti-EV71 effects by suppressing viral replication and release.

    Conclusions:

    • Total astragalosides (ASTs) exhibit protective effects against EV71-induced cell damage and programmed cell death.
    • ASTs suppress EV71 replication and release, indicating potential as an antiviral agent for EV71 infections.