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Background  Inflammatory 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.    Aim  The current study aimed to elucidate the potential role of CS in a 2,4,6‐trinitrobenzene sulfonic acid (TNBS)‐induced colitis model.    Methods  Male 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.    Results  TNBS‐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.    Conclusion  CS 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.

Cilostazol against 2,4,6‐trinitrobenzene sulfonic acid‐induced colitis: Effect on tight junction, inflammation, and apoptosis