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Chebulinic Acid Exerts Anti-rotavirus Effects through the p38MAPK/ERK1/2 Signaling Pathway.

Junxian Yu1, Didong Zhang1, Yupei Qian1

  • 1Dongguan Key Laboratory of Screening and Research of Anti-inflammatory Ingredients in Chinese Medicine, The First Dongguan Affiliated Hospital, School of Pharmacy, Guangdong Medical University, Dongguan, 523808, China.

Current Pharmaceutical Design
|April 20, 2026
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Summary
This summary is machine-generated.

Chebulinic acid (CA) effectively inhibits rotavirus (RV) by reducing viral protein expression and oxidative stress. This study demonstrates CA

Keywords:
Chebulinic acidERK1/2P38MAPKROSRV infection..Rotavirus

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Area of Science:

  • Virology
  • Pharmacology
  • Biochemistry

Background:

  • Rotavirus (RV) is a primary cause of severe diarrhea in young children, with no current clinical treatments.
  • Chebulinic acid (CA), a polyphenolic compound, is investigated for its potential anti-RV activity.

Purpose of the Study:

  • To evaluate the anti-rotavirus efficacy of chebulinic acid (CA).
  • To elucidate the underlying mechanism of CA's anti-RV action, focusing on oxidative stress and signaling pathways.
  • To assess CA's therapeutic potential in both in vitro and in vivo models.

Main Methods:

  • In vitro antiviral activity assessed via CCK8 assay, qRT-PCR, western blotting, and immunofluorescence.
  • In silico network pharmacology identified the p38/ERK axis as a key target.
  • ROS production and scavenging activity were measured; western blotting analyzed p38MAPK/ERK1/2 pathway inhibition.
  • In vivo efficacy tested using a rotavirus-infected zebrafish model.

Main Results:

  • CA (4-10 μmol/L) inhibited viral VP6 expression and decreased mitochondrial ROS production.
  • Network pharmacology identified 38 CA-RV targets, highlighting the p38 MAPK pathway.
  • CA downregulated p38MAPK/ERK1/2 phosphorylation, mitigating viral infection effects.
  • In zebrafish, CA improved survival rates, reduced convulsive behavior, and restored intestinal morphology by decreasing inflammation.

Conclusions:

  • CA demonstrates significant anti-rotavirus properties by inhibiting mitochondrial oxidation-induced apoptosis through the p38MAPK/ERK1/2 signaling pathway.
  • CA reverses RV-induced pathological alterations, offering a novel therapeutic strategy for rotavirus infections.
  • These findings support the potential clinical application of CA as an anti-rotavirus agent.