Evidence map›Paper›PMID 34231472›Full record

ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2021

Protection by microRNA-7a-5p Antagomir Against Intestinal Mucosal Injury Related to the JNK Pathway in TNBS-Induced Experimental Colitis.

Bao Yin, Huang Tian-Chu, Xu Ling-Fen

Open access · greenAbstract read
In one paragraph

Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Modulation of Oxidative Stress and Nuclear Factor-κB- Associated Inflammatory Signaling by Rabeprazole in Acetic Acid-Induced Colonic InjuryThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Bao YinDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China; Department of Rehabilitation, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China.
Huang Tian-ChuKey Laboratory of Congenital Malformation, Ministry of Health, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China.
Xu Ling-FenDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing 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.

methodsColitis 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.

resultsmiR-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.

conclusionThis 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.

Indexed as

AntagomirsAnimalsColitisDisease Models, AnimalInflammatory Bowel DiseasesIntestinal MucosaIntestinesMaleMAP Kinase Signaling SystemMiceMicroRNAsTrinitrobenzenesulfonic AcidAntagomirsMicroRNAsTrinitrobenzenesulfonic Acid

Identifiers

PMID34231472
PMCPMC8975295
OpenAlexW3175455932

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.