ArticleJournal of inflammation research2026
CD73 Blockade Aggravate Dextran-Sodium-Sulfate-Induced Colitis via Down Regulating Inosine.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: CD73, a pivotal enzyme in the purinergic signaling cascade, modulates the concentrations of adenosine and inosine. These metabolites are involved in immune responses and inflammatory processes. This study aims to investigate the function of CD73 in the pathogenesis of inflammatory bowel disease (IBD) and explore the potential mechanism. Methods: Dextran-Sodium-Sulfate (DSS)-induced colitis mice models were established by orally administering 3% DSS. CD73 was blocked by intraperitoneal injection of Adenosine 5'- (α, β-methylene) diphosphate (APCP). Inosine was supplemented by intraperitoneal injection. Hematoxylin-eosin (H&E), PAS and Alcian blue staining were used to evaluate the inflammation infiltration and colon damage. Serum IL-6 levels were detected by ELISA assay. High-performance liquid chromatography-mass spectrometry (LC-MS) was used to investigate the level of inosine. Results: Blockade of CD73 by APCP aggravated disease severity in DSS-induced colitis mice models, characterized by increased weight loss, colon shortening and pathological damage, increased disease activity and IL-6 production. Blocking CD73 impairs intestinal barrier function and integrity by reducing the expression of tight junction proteins (claudin-1, occludin and ZO-1), both in colon tissues and intestinal epithelial cell-MODE-K. In addition, APCP increased oxidative stress in colon tissue and MODE-K (increased MDA level, decreased SOD and GSH activities). Moreover, blocking CD73 reduced inosine levels in vivo and in vitro. We found that inosine treatment significantly ameliorated DSS-induced colitis in mice, as demonstrated by decreased weight loss, less colon shortening and histological injury, reduced disease activity and IL-6 production. Notably, the effects of inosine on MODE-K cells were opposite to those of APCP, including the effects on the expression of oxidative stress molecules and tight junction proteins. Conclusion: This study indicates that CD73 exerts a protective effect in the progress of DSS-induced colitis. Inosine supplementation might be a potential therapeutic strategy for colitis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.