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  2. Notoginsenoside R1 Inhibits Porcine Deltacoronavirus Infection In Vitro By Restoring Serca2-mediated Calcium Homeostasis.
  1. Home
  2. Notoginsenoside R1 Inhibits Porcine Deltacoronavirus Infection In Vitro By Restoring Serca2-mediated Calcium Homeostasis.

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Notoginsenoside R1 Inhibits Porcine Deltacoronavirus Infection In Vitro by Restoring SERCA2-Mediated Calcium

Jialu Zhang1, Yuqian Liu1, Wenzhe Liu1

  • 1Joint International Research Laboratory of Animal Health and Animal Food Safety, College of Veterinary Medicine, Southwest University, Chongqing 400715, China.

Animals : an Open Access Journal From MDPI
|June 26, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Notoginsenoside R1 (NG-R1) effectively combats porcine coronavirus (PDCoV) by restoring calcium balance and reducing ER stress. This natural compound shows promise as a novel antiviral agent for swine health.

Keywords:
Notoginsenoside R1cellular calcium ionsendoplasmic reticulumporcine deltacoronavirus

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Area of Science:

  • Veterinary Virology
  • Natural Product Chemistry
  • Molecular Pharmacology

Background:

  • Porcine coronavirus (PDCoV) causes significant economic losses in the pig industry due to severe diarrhea in piglets.
  • Current antiviral strategies against PDCoV are limited, necessitating the exploration of new therapeutic agents.

Purpose of the Study:

  • To investigate the antiviral effects of Notoginsenoside R1 (NG-R1) against PDCoV.
  • To elucidate the underlying molecular mechanisms of NG-R1's antiviral activity.

Main Methods:

  • Cell viability assays using LLC-PK1 cells.
  • Network pharmacology analysis to identify potential pathways.
  • Intracellular calcium level measurements and endoplasmic reticulum (ER) stress assessment.
  • Analysis of SERCA2 expression and functional assays with SERCA2 inhibitor.

Main Results:

  • NG-R1 demonstrated no cytotoxicity and inhibited PDCoV replication throughout its life cycle.
  • PDCoV infection disrupted calcium homeostasis and induced ER stress, which NG-R1 partially reversed.
  • NG-R1 modulated SERCA2 expression, and SERCA2 inhibition mimicked NG-R1's antiviral effect.

Conclusions:

  • NG-R1 possesses significant antiviral activity against PDCoV.
  • The mechanism involves the regulation of intracellular calcium homeostasis via SERCA2, thereby attenuating ER stress.
  • NG-R1 represents a potential therapeutic candidate for PDCoV infections, targeting calcium signaling pathways.