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Published on: January 7, 2019
MiR-146a regulates the development of ulcerative colitis via mediating the TLR4/MyD88/NF-κB signaling pathway
1Department of Gastroenterology, Shanxi Provincial People's Hospital, The Affiliated People's Hospital of Shanxi Medical University, Taiyuan, China. wangjp8396@126.com.
Objective:
To study the effect of micro ribonucleic acid (miR)-146a on the development of ulcerative colitis (UC) and to explore its regulatory effect on the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) and nuclear factor-kappa B (NF-κB) signaling pathways.
Materials And Methods:
The UC model in rats was established using 2,4,6-trinitrobenzenesulfonic acid (TNBS)/ethanol. A total of 30 male rats were randomly divided into control group, model group and miR-146a inhibitor group, with 10 rats in each group. The disease activity index (DAI) and the macroscopic score of colonic mucosa were measured in each rat. MiR-146a expression in rat intestinal tissues was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Serum levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Additionally, Western blotting assay was performed to detect protein levels of TLR4, MyD88, and NF-κB in rat intestinal tissues.
Results:
Compared with those in control group, rats in model group had notably increased DAI, inflammation score, upregulated expression levels of TLR4, MyD88, NF-κB, and miR-146a, as well as increased serum levels of IL-1β and TNF-α. However, rats in miR-146a inhibitor group exhibited substantially decreased DAI, inflammation score, lowered content of IL-1β and TNF-α and levels of TLR4, MyD88, and NF-κB compared with those in model group.
Conclusions:
We found that miR-146a inhibitor alleviates UC by reducing the release of inflammatory factors through suppressing the TLR4/MyD88/NF-κB signaling pathway.
Insights
Micro ribonucleic acid (miR)-146a inhibition alleviates ulcerative colitis (UC) by reducing inflammatory factors. This occurs through the suppression of the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
- The role of microRNAs (miRNAs) in UC pathogenesis is increasingly recognized.
- Specific miRNAs, like miR-146a, may regulate key inflammatory pathways implicated in UC.
Purpose of the Study:
- To investigate the impact of miR-146a on the development of ulcerative colitis (UC).
- To elucidate the regulatory role of miR-146a in the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signaling cascade.
Main Methods:
- A rat model of UC was induced using TNBS/ethanol.
- Rats were divided into control, model, and miR-146a inhibitor groups.
- Disease activity index, colonic mucosal scores, miR-146a expression, inflammatory cytokine levels (IL-1β, TNF-α), and protein expression of TLR4, MyD88, and NF-κB were assessed.
Main Results:
- UC induction led to increased disease activity, inflammation, miR-146a expression, IL-1β, TNF-α, TLR4, MyD88, and NF-κB.
- Administration of a miR-146a inhibitor significantly reduced disease activity, inflammation, IL-1β, TNF-α, TLR4, MyD88, and NF-κB levels.
Conclusions:
- miR-146a plays a significant role in the development of ulcerative colitis.
- Inhibiting miR-146a demonstrates therapeutic potential for UC.
- The therapeutic effect is mediated by the suppression of the TLR4/MyD88/NF-κB signaling pathway and subsequent reduction in inflammatory factors.
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