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Related Experiment Video

Updated: Aug 11, 2025

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

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Published on: January 5, 2017

Ginsenoside Rg3 Ameliorates DSS-Induced Colitis by Inhibiting NLRP3 Inflammasome Activation and Regulating Microbial

Dongcai Liu¹, Qingquan Tian², Kuijie Liu¹

¹General Surgery Department, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Journal of Agricultural and Food Chemistry

|February 8, 2023

Summary

Ginsenoside Rg3 effectively treats ulcerative colitis (UC) by reducing inflammation and restoring gut bacteria balance. This natural compound inhibits NLRP3 inflammasome activation, offering a potential therapeutic strategy for UC.

Keywords:

NLRP3 ginsenoside Rg3 gut microbiota microbial metabolism ulcerative colitis

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Published on: February 27, 2014

Area of Science:

Gastroenterology
Immunology
Pharmacology

Background:

Ulcerative colitis (UC) is a chronic inflammatory condition lacking definitive treatments.
Inflammasome activation, particularly NLRP3, plays a critical role in UC pathogenesis.
Gut microbiota dysbiosis is a key feature of UC.

Purpose of the Study:

To investigate the therapeutic potential of ginsenoside Rg3 (Gin Rg3) in ulcerative colitis.
To elucidate the underlying mechanisms of Gin Rg3 action, focusing on NLRP3 inflammasome and gut microbiota.

Main Methods:

Established in vitro cellular inflammation and dextran sulfate sodium (DSS)-induced UC mouse models.
Intervention with Gin Rg3, NLRP3 inhibitor (MCC950), NLRP3 activator (MSU), and fecal microbiota transplantation (FMT).
Assessed NLRP3 inflammasome activation, pyroptosis, apoptosis, gut microbiota composition, and intestinal metabolism.

Main Results:

Gin Rg3 significantly inhibited NLRP3 inflammasome activation, pyroptosis, and apoptosis in both in vitro and in vivo models.
Gin Rg3 partially restored DSS-induced gut microbiota dysbiosis.
Gin Rg3 treatment modulated intestinal metabolism by suppressing NLRP3 inflammasome activation.

Conclusions:

Ginsenoside Rg3 demonstrates significant therapeutic effects in alleviating DSS-induced UC.
The mechanism involves the inhibition of NLRP3 inflammasome activation and the regulation of gut microbiota homeostasis.
Gin Rg3 represents a promising natural compound for UC treatment.