The pathogenesis of inflammatory bowel disease (IBD) is believed to be associated with the abnormal expression of inflammatory factors. The
aryl hydrocarbon receptor (AhR) is a ligand‑dependent
transcription factor, which can suppress the inflammatory response and attenuate experimental
colitis. However, the detailed mechanism underlying the effects of AhR remains unclear. The present study investigated the role of AhR in the pathogenesis of IBD.
Colitis was induced in mice by administration of 3%
dextran sulphate
sodium (DSS) for 7 days. The mice were also administered
injections of the AhR agonist, 6‑formylindolo(3,2‑b)carbazole (
FICZ), starting 2 days after the first administration of DSS. Furthermore, LoVo cells were treated with
lipopolysaccharide (LPS) in the presence or absence of
FICZ for 8 h. The
protein expression levels of AhR,
cytochrome P450 1A1 (
CYP1A1) and tristetraprolin (
TTP) were assessed by western blotting and immunofluorescence, whereas
mRNA expression levels were assessed by reverse transcription‑quantitative polymerase chain reaction. The results indicated that injection of mice with
FICZ significantly attenuated DSS‑induced
colitis; in addition, the expression levels of inflammatory
cytokines were markedly downregulated. Conversely, the expression levels of AhR and
TTP were upregulated. In addition, mice in the AhR‑knockout + DSS group exhibited elevated inflammatory
cytokine production and developed more severe
colitis. In LoVo cells, incubation with
FICZ decreased the expression levels of inflammatory
cytokines, whereas AhR and
TTP expression was increased. In addition, the levels of phosphorylated‑mitogen‑activated
protein kinase‑activated
protein kinase 2 (p‑MK2) were decreased. These results suggested that AhR deficiency resulted in increased susceptibility to
colitis, whereas activation of AhR by
FICZ could ameliorate DSS‑induced
colitis via the MK2/p‑MK2/
TTP pathway.