ArticleJGH open : an open access journal of gastroenterology and hepatology2019
Cilostazol against 2,4,6-trinitrobenzene sulfonic acid-induced colitis: Effect on tight junction, inflammation, and apoptosis.
Article in JGH open : an open access journal of gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Rectal roflumilast improves trinitrobenzenesulfonic acid-induced chronic colitis in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022Article
- Could cilostazol be beneficial in COVID-19 treatment? Thinking about phosphodiesterase-3 as a therapeutic target.International immunopharmacology · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory bowel diseases are immunologically mediated disorders of gastrointestinal tract, characterized by dysregulated immune responses that result in a chronic intestinal inflammation. The antiplatelet cilostazol (CS), a phosphodiesterase-III inhibitor, exerted a beneficial effect on several models of gastrointestinal diseases; however, the full mechanism of action in this context has not been unveiled.
aimThe current study aimed to elucidate the potential role of CS in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model.
methodsMale Wistar rats were divided into a sham group and groups treated with sulfasalazine (500 mg/kg), CS (50 and 100 mg/kg), and a combination (sulfasalazine/CS 50 mg/kg). All treatments were administered orally 15 days, with TNBS rectal administration on the 11th day.
resultsTNBS-produced colitis manifested as a decrease in the epithelial junctional adhesion molecule-A (JAM-A) and as an increase in trefoil factor-3, ulcerative area, and colon mass index, parameters that collaborate with the gross macroscopic changes in colon tissue. In addition, TNBS increased hemeoxygenase-1, nuclear factor-kappa B, P-selectin, and myeloperoxidase, as well as the apoptotic ratio of Bax/Bcl-2. Administration of CS alone, especially at the high dose level, attenuated the severity of TNBS-induced colitis in a sulfasalazine-comparable manner. In addition, a better effect was mediated by the combination regimen, which succeeded in normalizing most of the measured parameters.
conclusionCS protected the colon against TNBS through its anti-inflammatory and antiapoptotic effects along with maintaining cellular tight junctions (TJs). Furthermore, CS can be beneficial as an add-on drug with the conventional treatments of colitis.
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