Downregulation of miR-23b-3p improves the intestinal mucosal barrier function in LPS-induced intestinal epithelial...

Inflammatory bowel disease (IBD) is a persistent inflammation of the gastrointestinal tract that severely affects patients' quality of life. miRNAs are associated with the pathogenesis of IBD. Nevertheless, the mechanism of miR-23b-3p and IBD has yet to be elucidated. The aim of this study was to investigate the potential clinical diagnostic value of miR-23b-3p and its related molecular mechanisms. LPS was utilized to construct an LPS-induced intestinal epithelial inflammatory injury model in vitro. RT-qPCR was employed to measure the levels of miR-23b-3p and Erbin. The MTT assay was applied to detect cell viability. ELISA was performed to monitor the inflammation factor levels. The fluorescein isothiocyanate-dextran assay was employed to assess permeability. Dual-luciferase reporter assay was performed to validate the targeting relationship. The level of miR-23b-3p was elevated in patients with ulcerative colitis (UC) and Crohn's disease (CD) and it showed promising diagnostic ability for IBD. Furthermore, miR-23b-3p showed positive correlations with the Mayo score in UC patients and the CDAI score in CD patients. In terms of mechanism, miR-23b-3p inhibitor enhanced cell viability and TEER as well as reduced proinflammatory factor levels and FITC-dextran permeability in the LPS-induced intestinal epithelial inflammatory injury model, which was reversed by si-Erbin. These findings suggest that miR-23b-3p may contribute to intestinal epithelial inflammatory injury and barrier dysfunction, at least partly through regulation of Erbin.

The online version contains supplementary material available at 10.1007/s10616-026-01050-3.