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Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model
Published on: February 14, 2021
Cilostazol against 2,4,6-trinitrobenzene sulfonic acid-induced colitis: Effect on tight junction, inflammation, and
Hiba A Al-Kishali1, Mai A Abd El Fattah1, Waleed A Mohammad2
1Department of Pharmacology and Toxicology, Faculty of Pharmacy Cairo University Cairo Egypt.
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.
Insights
Cilostazol (CS) effectively treats colitis by reducing inflammation and apoptosis, preserving gut barrier integrity. This study shows CS is a promising add-on therapy for inflammatory bowel diseases.
Area of Science:
- Gastroenterology
- Pharmacology
- Immunology
Background:
- Inflammatory bowel diseases (IBD) involve chronic intestinal inflammation due to immune dysregulation.
- Cilostazol (CS), a phosphodiesterase-III inhibitor, shows promise in gastrointestinal disease models, but its mechanism in IBD is unclear.
Purpose of the Study:
- To investigate the therapeutic potential of CS in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model in rats.
- To elucidate the anti-inflammatory and protective mechanisms of CS in colitis.
Main Methods:
- Rats with TNBS-induced colitis were treated with sulfasalazine, CS (50 and 100 mg/kg), or a combination therapy.
- Treatments were administered orally for 15 days, with TNBS administered rectally on day 11.
- Key parameters assessed included epithelial integrity, inflammatory markers, and apoptosis.
Main Results:
- TNBS-induced colitis increased ulcerative area, colon mass index, inflammatory markers (NF-κB, myeloperoxidase), and apoptosis (Bax/Bcl-2 ratio).
- CS treatment, particularly at a high dose, significantly reduced colitis severity, comparable to sulfasalazine.
- Combination therapy demonstrated superior efficacy, normalizing most measured parameters and maintaining epithelial junctional adhesion molecule-A (JAM-A).
Conclusions:
- CS exhibits anti-inflammatory and antiapoptotic effects, protecting the colon against TNBS-induced injury.
- CS helps maintain cellular tight junctions (TJs), crucial for gut barrier function.
- CS holds potential as an effective add-on therapy for conventional colitis treatments.
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