Abstract
Ferroptosis is a form of iron-dependent lipid peroxidation cell death that plays an important role in inflammation. However, the mechanism of ferroptosis in ulcerative colitis (UC) remains to be further investigated. In the present study, we merged the differentially expressed genes (DEGs) of UC in GEO database with the ferroptosis-related genes of FerrDb for bioinformatics analysis and successfully screened out the ferroptosis-related hub gene STAT3 (signal transducer and activator of transcription 3). Then we further validated the role of STAT3-mediated ferroptosis in vitro and in vivo models of colitis. The results showed that ferroptosis was increased in DSS-induced colitis, salmonella typhimurium (S. Tm) colitis and H2O2-induced IEC-6 cells. And the phosphorylation level of the hub gene STAT3 was down-regulated in IEC-6 cells treated with H2O2, while Fer-1, an ferroptosis inhibitor, reactivated the phosphorylation level of STAT3. In addition, co-treatment of cells with H2O2 and STAT3 inhibitor (stattic) showed an additive effect on the extent of ferroptosis. Taken together, these findings suggest that ferroptosis is closely associated with the development of colitis and ferroptosis-related gene STAT3 could serve as a potential biomarker for diagnosis and treatment of ulcerative colitis.
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