Metformin attenuates colitis via blocking STAT3 acetylation by reducing acetyl-CoA production.

ABSTRACT:

Background and aims

While metformin has been shown to alleviate dextran sulfate sodium (DSS)-induced colitis in murine models, the mechanisms underlying its anti-inflammatory and barrier-restorative effects remain poorly defined. This study investigates the role of acetyl coenzyme A (acetyl-CoA)-dependent STAT3 acetylation in mediating metformin's therapeutic actions, with the goal of identifying novel molecular targets for ulcerative colitis (UC) treatment.

Methods

Acute colitis was induced in wild-type C57BL/6J mice via oral DSS administration, followed by daily intraperitoneal metformin treatment. Intestinal inflammation, barrier integrity, and STAT3 signaling were assessed using histopathology, western blotting, and transmission electron microscopy. To validate STAT3's c

SUBMITTER: Li X 

PROVIDER: S-EPMC12766235 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature