Gastrointestinal Tract - Original Article
Vol. 32 No. 5 (2021): 2021.32.5-Turkish Journal of Gastroenterology
Protection by microRNA-7a-5p Antagomir Against Intestinal Mucosal Injury Related to the JNK Pathway in TNBS-Induced Experimental Colitis
Main Article Content
Abstract
Background: Increasing evidence shows that microRNA-7a-5p (miR-7a-5p) plays an important role in regulating the inflammatory process in inflammatory bowel disease (IBD). How miR-7a-5p contributes to this process is poorly defined. The purpose of this study was to examine whether miR-7a-5p regulates 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced inflammatory responses via the JNK pathway.<br>
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Methods: Colitis was induced in male mice by intracolonic administration of TNBS; mice were divided into 3 groups: normal control (NC), TNBS, and miR-7a-5p antagomir-treated group. Inflammatory responses were estimated by disease activity index (DAI) and histological scores. The relative expressions of miR-7a-5p and tight junction protein, ZO-1, were detected by RT-qPCR. Western blot assays were used to estimate the level of JNK pathway proteins and ZO-1. After miRNA-antagomir injection, the extent of colonic tissue injury and expression levels of ZO-1 and JNK in intestinal tissue were compared.<br>
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Results: miR-7a-5p and p-JNK expression were higher in the intestinal tissue of the TNBS group as compared to NC. Inhibition of the expression of miR-7a-5p resulted in significantly decreased expression of p-JNK but increased expression of ZO-1 and promoted the recovery of intestinal mucosa.<br>
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Conclusion: This work demonstrates a correlation between the JNK pathway and miR-7a-5p in TNBS-induced experimental colitis in mice, which may provide a new research direction for the treatment of IBD.<br>
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Cite this article as: Bao Y, Huang TC, Xu LF. Protection by microRNA-7a-5p antagomir against intestinal mucosal injury related to the JNK pathway in TNBS-induced experimental colitis. Turk J Gastroenterol. 2021; 32(5): 431-436.
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Methods: Colitis was induced in male mice by intracolonic administration of TNBS; mice were divided into 3 groups: normal control (NC), TNBS, and miR-7a-5p antagomir-treated group. Inflammatory responses were estimated by disease activity index (DAI) and histological scores. The relative expressions of miR-7a-5p and tight junction protein, ZO-1, were detected by RT-qPCR. Western blot assays were used to estimate the level of JNK pathway proteins and ZO-1. After miRNA-antagomir injection, the extent of colonic tissue injury and expression levels of ZO-1 and JNK in intestinal tissue were compared.<br>
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Results: miR-7a-5p and p-JNK expression were higher in the intestinal tissue of the TNBS group as compared to NC. Inhibition of the expression of miR-7a-5p resulted in significantly decreased expression of p-JNK but increased expression of ZO-1 and promoted the recovery of intestinal mucosa.<br>
<br>
Conclusion: This work demonstrates a correlation between the JNK pathway and miR-7a-5p in TNBS-induced experimental colitis in mice, which may provide a new research direction for the treatment of IBD.<br>
<br>
Cite this article as: Bao Y, Huang TC, Xu LF. Protection by microRNA-7a-5p antagomir against intestinal mucosal injury related to the JNK pathway in TNBS-induced experimental colitis. Turk J Gastroenterol. 2021; 32(5): 431-436.