Effect of Triptolide on Dextran Sodium Sulfate-Induced Ulcerative Colitis and Gut Microbiota in Mice

Hao Wu1, Quan Rao1,2, Guang-Chao Ma1

  • 1The Department of General Surgeryis a part of Beijing Friendship Hospital, Capital Medical University, Beijing, China.

Frontiers in Pharmacology
|February 18, 2020
PubMed

Insights

Triptolide effectively treats ulcerative colitis (UC) by restoring gut microbiota balance. This study shows triptolide improves microbial diversity and composition in UC mice, offering a new therapeutic approach.

Area of Science:

  • Gastroenterology
  • Microbiology
  • Pharmacology

Background:

  • Ulcerative colitis (UC) is linked to gut microbiota dysbiosis.
  • Triptolide shows potential for UC treatment, but its impact on gut microbiota is unknown.

Purpose of the Study:

  • To investigate the therapeutic effects of triptolide on dextran sodium sulfate (DSS)-induced UC in mice.
  • To determine if triptolide modulates the gut microbiota composition and diversity during UC treatment.

Main Methods:

  • Established DSS-induced UC mouse models.
  • Analyzed gut microbiota changes using high-throughput sequencing.
  • Assessed therapeutic effects of triptolide and performed fecal microbiota transplantation.

Main Results:

  • Triptolide demonstrated anti-inflammatory and therapeutic effects in UC mice.
  • DSS induced gut microbiota disorder and decreased microbial diversity.
  • Triptolide treatment restored microbial diversity and accelerated microbiota recovery.
  • Triptolide altered the abundance of specific bacterial phyla (e.g., decreased Bacteroidetes, increased Firmicutes) and genera (e.g., decreased Bacteroides, Lachnospiraceae).
  • Fecal transplantation from triptolide-treated mice alleviated UC symptoms.

Conclusions:

  • Triptolide regulates gut microbiota composition and diversity in UC mice.
  • Triptolide accelerates microbiota recovery, contributing to its therapeutic effects in UC.
  • Fecal microbiota transplantation further supports triptolide's efficacy, suggesting a microbiota-mediated mechanism.