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MiR-146a regulates the development of ulcerative colitis via mediating the TLR4/MyD88/NF-κB signaling pathway.
Eur Rev Med Pharmacol Sci. 2019 Mar; 23(5):2151-2157.ER

Abstract

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.

Authors+Show Affiliations

Department of Gastroenterology, Shanxi Provincial People's Hospital, The Affiliated People's Hospital of Shanxi Medical University, Taiyuan, China. wangjp8396@126.com.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30915760

Citation

Wang, J-P, et al. "MiR-146a Regulates the Development of Ulcerative Colitis Via Mediating the TLR4/MyD88/NF-κB Signaling Pathway." European Review for Medical and Pharmacological Sciences, vol. 23, no. 5, 2019, pp. 2151-2157.
Wang JP, Dong LN, Wang M, et al. MiR-146a regulates the development of ulcerative colitis via mediating the TLR4/MyD88/NF-κB signaling pathway. Eur Rev Med Pharmacol Sci. 2019;23(5):2151-2157.
Wang, J. P., Dong, L. N., Wang, M., Guo, J., & Zhao, Y. Q. (2019). MiR-146a regulates the development of ulcerative colitis via mediating the TLR4/MyD88/NF-κB signaling pathway. European Review for Medical and Pharmacological Sciences, 23(5), 2151-2157. https://doi.org/10.26355/eurrev_201903_17260
Wang JP, et al. MiR-146a Regulates the Development of Ulcerative Colitis Via Mediating the TLR4/MyD88/NF-κB Signaling Pathway. Eur Rev Med Pharmacol Sci. 2019;23(5):2151-2157. PubMed PMID: 30915760.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MiR-146a regulates the development of ulcerative colitis via mediating the TLR4/MyD88/NF-κB signaling pathway. AU - Wang,J-P, AU - Dong,L-N, AU - Wang,M, AU - Guo,J, AU - Zhao,Y-Q, PY - 2019/3/28/entrez PY - 2019/3/28/pubmed PY - 2020/8/14/medline SP - 2151 EP - 2157 JF - European review for medical and pharmacological sciences JO - Eur Rev Med Pharmacol Sci VL - 23 IS - 5 N2 - 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. SN - 2284-0729 UR - https://www.unboundmedicine.com/medline/citation/30915760/MiR_146a_regulates_the_development_of_ulcerative_colitis_via_mediating_the_TLR4/MyD88/NF_κB_signaling_pathway_ L2 - https://www.europeanreview.org/article/17260 DB - PRIME DP - Unbound Medicine ER -