MiR-195 alleviates ulcerative colitis in rats via MAPK signaling pathway.

Abstract

To study the effect of micro ribonucleic acid (miR)-195 on the inflammatory response of ulcerative colitis (UC) model rats and to explore its regulatory mechanism, thus providing a new scheme for the clinical treatment of UC. A rat model of UC was prepared by 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)/ethanol assay, and the rats were randomly divided into Control group, Model group, and miR-195 mimic (miR-195 agomir) group. The disease activity index (DAI) in each group was observed. Hematoxylin and eosin (H&E) staining was utilized to detect the pathological changes in the rat colon tissues in each group. The levels of interleukin-6 (IL-6) and IL-1β in the colon tissues of the rats in each group were detected by enzyme-linked immunosorbent assay (ELISA). In addition, the messenger RNA (mRNA) and protein levels of p38 mitogen-activated protein kinase (p38 MAPK) and tumor necrosis factor-alpha (TNF-α) in the colon tissues of each group of rats were examined via Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting, respectively. Compared with those in Control group, the rats in Model group had an increased DAI score, severely pathologically damaged colon tissues, raised levels of IL-6 and IL-1β in the colon tissues and significantly elevated mRNA and protein levels of p38 MAPK and TNF-α. In comparison with those in Model group, the DAI score was decreased, the pathological damage to the rat colon tissues was improved, the levels of IL-6 and IL-1β in the rat colon tissues were reduced, and the mRNA and protein levels of p38 MAPK and TNF-α were notably lowered in miR-195 agomir group. MiR-195 mimics can alleviate the pathological damage to the colon and inflammatory responses in UC model rats, and its mechanism may be related to the inhibition on the p38 MAPK signaling pathway.