miRNA-301 As a molecule promoting necrotizing enterocolitis by inducing inflammation

  • Dajun Zou Department of Pediatric Surgery, Affiliated Hospital of Chengde Medical College, 36 Nanyingzi Street, Chengde, Hebei, 067000. P.R. China
  • Fude Hu Department of Pediatric Surgery, Affiliated Hospital of Chengde Medical College, 36 Nanyingzi Street, Chengde, Hebei, 067000. P.R. China
  • Qili Zhou Department of Pediatric Surgery, Affiliated Hospital of Chengde Medical College, 36 Nanyingzi Street, Chengde, Hebei, 067000. P.R. China
  • Xiaoqing Xu Department of Pediatric Surgery, Affiliated Hospital of Chengde Medical College, 36 Nanyingzi Street, Chengde, Hebei, 067000. P.R. China https://orcid.org/0000-0002-6441-0100

Abstract

Objective: Necrotizing enterocolitis (NEC) is a devastating inflammatory disease with high morbidity and mortality, mainly affecting premature infants. This study aimed to explore the role of miRNA-301a in the pathogenesis of NEC. Methods: The differentially expressed miRNAs and mRNAs were screened by collating RNA-Seq data from the GEO database of intestinal tissue samples. The differential miRNA-mRNAs regulatory network was constructed based on functional enrichment analysis. Newborn BALB/c mice were used to establish the NEC model. Haematoxylin and eosin staining was used to assess intestinal damage. The levels of IL-8 and TNF-α in mouse serum were evaluated by ELISA. qRT-PCR was used to detect the expression of miRNA-301a in intestinal tissues. Results: Bioinformatics analysis showed that miRNA-301a was involved in intestinal lesions. Intestinal tissue damage was reduced and serum levels of the inflammatory cytokines IL-8 and TNF-α were lower in NEC model mice treated with miRNA-301a antagonists. The level of miRNA-301a in intestinal tissues of NEC model mice was significantly higher than in the control group and miRNA-301a antagonists treated group. Conclusion: miRNA-301a plays an important role in the pathogenesis of NEC by promoting inflammation, and is a potential therapeutic target of NEC.

Published
2023-11-28
Section
Articles