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Related Experiment Video

Updated: Jan 10, 2026

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Berberine Repairs Intestinal Mucosal Barrier by Targeting HSP90AA1 and MAPK14.

Danya Zhao1, Yang Zhai2, Chen Chen3

  • 1Department of Gastroenterology, Hangzhou Red Cross Hospital/Hospital of Integrated Chinese and Western Medicine, Hangzhou, People's Republic of China.

Pharmacogenomics and Personalized Medicine
|November 24, 2025
PubMed
Summary

Berberine (BBR) may treat Crohn's disease by targeting HSP90AA1 and MAPK14. This natural compound repairs the intestinal barrier, reducing inflammation and improving symptoms in preclinical models.

Keywords:
Crohn’s diseaseMendelian randomizationberberineexperimental validationmolecular dynamics

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Area of Science:

  • Pharmacology
  • Gastroenterology
  • Molecular Biology

Background:

  • Berberine (BBR), derived from Coptis chinensis, exhibits diverse pharmacological effects.
  • Its precise therapeutic targets and mechanisms in Crohn's disease (CD) remain largely unelucidated.

Purpose of the Study:

  • To identify the molecular targets and mechanisms of BBR in Crohn's disease (CD) treatment.
  • To evaluate the therapeutic efficacy of BBR in preclinical models of CD.

Main Methods:

  • Network pharmacology, Mendelian randomization (MR), molecular docking, and molecular dynamics simulations were utilized.
  • In vitro assays assessed BBR's effects on cellular models of inflammation.
  • In vivo studies evaluated BBR's efficacy in a dextran sulfate sodium (DSS)-induced mouse model of colitis.

Main Results:

  • Heat shock protein 90 kDa alpha class A member 1 (HSP90AA1) and mitogen-activated protein kinase 14 (MAPK14) were identified as key targets of BBR in CD.
  • BBR downregulated lipopolysaccharide (LPS)-induced HSP90AA1, MAPK14, and tumor necrosis factor-alpha (TNF-α) expression.
  • BBR treatment restored intestinal tight junction proteins (ZO-1, Occludin, Claudin-1, JAM-A) and ameliorated DSS-induced colitis symptoms in mice.

Conclusions:

  • Berberine (BBR) effectively inhibits HSP90AA1 and MAPK14 expression in both in vitro and in vivo models.
  • These inhibitory actions facilitate the repair of the intestinal mucosal barrier, offering a potential therapeutic strategy for Crohn's disease.