The Effect of GB1 on DSS-Induced Colitis in WT and Nlrp3-/- Mice

TL;DR

This study shows that GB1 reduces colitis symptoms in mice by suppressing inflammation and restoring intestinal barriers.

Contribution

The novel finding is that GB1's protective effects against colitis depend on the NLRP3 inflammasome pathway.

Findings

GB1 reduced colitis symptoms in wild-type mice by suppressing pro-inflammatory mediators and NLRP3 inflammasome components.

GB1's effects were absent in Nlrp3-/- mice, confirming the role of NLRP3 in its mechanism.

GB1 improved intestinal barrier integrity and reduced mucosal inflammation.

Abstract

This study investigated the protective effects of Garcinia biflavonoid 1 (GB1) against dextran sulfate sodium (DSS)-induced ulcerative colitis and its underlying mechanisms. Using wild-type (WT) and NLRP3 knockout (Nlrp3-/-) mice, we demonstrated that GB1 administration significantly ameliorated colitis symptoms, as evidenced by improved body weight, disease activity index (DAI) scores, colon length, and histological damage in WT mice. Mechanistically, GB1 downregulated pro-inflammatory mediators (IL-6, NF-κB, and CD11b) while attenuating the expression of NLRP3 inflammasome components (ASC, Caspase-1, and IL-1β). Notably, these protective effects were abolished in Nlrp3-/- mice, confirming the essential role of NLRP3 in GB1-mediated mitigation of colitis. Furthermore, GB1 reinforced intestinal barrier integrity by preserving tight junctions, reducing permeability, and attenuating mucosal inflammation. Collectively, our findings highlight GB1 as a promising therapeutic candidate for colitis treatment, primarily through NLRP3 inflammasome suppression and intestinal barrier restoration.

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