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Surgical Research and New Technique ›› 2025, Vol. 14 ›› Issue (3): 204-210.doi: 10.3969/j.issn.2095-378X.2025.03.002

• Original article • Previous Articles     Next Articles

Role and mechanism of miR-21-5p in early adverse life events inducing irritable bowel syndrome

ZHANG Haiqin1, HAN Bo2, ZHOU Lu1, CHU Yimin1, XU Ying1, PENG Haixia1   

  1. 1. Digestive Endoscopy Center, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China;
    2. Department of General Surgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
  • Received:2024-12-02 Online:2025-09-28 Published:2025-10-17

Abstract: Objective To investigate the role of miR-21-5p in early adverse life events (EALs)-induced visceral hypersensitivity of irritable bowel syndrome (IBS) and its mechanism. Methods A rat model of visceral hypersensitivity induced by EALs in adult rats was established by mother-infant separation. MicroRNA (miRNA) microarrays combined with quantitative polymerease chain reaction (qPCR) were used to screen for differential miRNAs in dorsal root ganglion (DRG) neurons, and bioinformatics analysis combined with luciferase reporter gene assay was performed to search for downstream targets of the differential miRNAs. Cellular and animal experiments were combined to verify if the differential miRNAs were involved in mother-infant separation-induced visceral hypersensitivity through the downstream targets. Results MiR-21-5p was significantly overexpressed in the DRG neurons of mother-infant separation-induced adult visceral hypersensitivity rats (P<0.05). Bioinformatics analysis, luciferase reporter gene assay, and cellular experiments suggested that transforming growth factor beta induction (TGFBI) gene was a miR-21-5p target gene. At the cellular level, the TGFBI protein level in DRG neurons was significantly decreased after miR-21-5p mimic intervention (P<0.05), and significantly increased after miR-21-5p inhibitor intervention (P<0.05). At the animal level, the visceral sensitivity was significantly higher (P<0.05) and TGFBI protein level was significantly lower (P<0.05) in rats after miR-21-5p agonist intervention compared with the control group,and visceral sensitivity was significantly lower (P<0.05) and the TGFBI protein level was significantly higher (P<0.05) in rats after miR-21-5p antagonist intervention compared with the control group. Conclusion MiR-21-5p in rat DRG promotes mother-infant separation-induced visceral hypersensitivity by inhibiting TGFBI expression, and thus participates in the development of adult IBS induced by EALs.

Key words: Irritable bowel syndrome, Visceral hypersensitivity, MiR-21-5p, Transforming growth factor beta induction, Early adverse life events

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