MPST deficiency promotes intestinal epithelial cell apoptosis and aggravates inflammatory bowel disease via AKT.

ABSTRACT:

Background & aims

Excessive inflammatory responses and oxidative stress are considered the main characteristics of inflammatory bowel disease (IBD). Endogenous hydrogen sulfide (H₂S) has been reported to show anti-inflammatory activity in IBD. The main aim of this study was to explore the role of 3-mercaptopyruvate sulfurtransferase (MPST), a key enzyme that regulates endogenous H₂S biosynthesis, in IBD.

Methods

Colonic MPST expression was evaluated in mice and patients with IBD. Various approaches were used to explore the concrete mechanism underlying MPST regulation of the progression of colitis through in vivo and in vitro models.

Results

MPST expression was markedly decreased in colonic samples from patients with ulcerative colitis (UC) or Cr

SUBMITTER: Zhang J 

PROVIDER: S-EPMC9486620 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature