Aim: To explore the effects of miR-141-3p on intestinal epithelial cells in necrotizing enterocolitis and the underlying mechanism.

Results: The expression of miR-141-3p was significantly downregulated in serum samples of patients with NEC and LPS-treated Caco-2 cells. The in vitro assays showed that miR-141-3p mimics inhibited expression of IL-6 and TNF-α and reduced PI positive rate of the LPS-treated Caco-2 cells. Next, receptor interacting protein kinase 1 (RIPK1) was identified as the downstream molecule of miR-141-3p, and RIPK1 overexpression aggravated LPS-induced Caco-2 cell injury, which was ameliorated by miR-141-3p mimics. Finally, we found miR-141-3p mimics inhibited upregulation of necroptosis-related molecules and interaction of RIPK1 and RIPK3 in LPS-treated Caco-2 cells.

Conclusion: Our research indicated that miR-141-3p protected intestinal epithelial cells from LPS damage by suppressing RIPK1-mediated inflammation and necroptosis, providing an alternative perspective to explore the pathogenesis of NEC.

Methods: Quantitative real time-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-141-3p in serum samples of participants and lipopolysaccharide (LPS)-treated Caco-2 cells. Cell Counting Kit-8 (CCK-8) assay, Propidium Iodide (PI) staining and detection of inflammatory cytokines were performed to evaluate the role of miR-141-3p in LPS-treated Caco-2 cells. TargetScanHuman database and luciferase reporter gene assay were utilized to confirm the direct downstream molecule of miR-141-3p. Western blot analysis was used to explore the mechanism.