Protective Effects of Oxytocin on Experimental Colitis: Modulation of Cytokines, Oxidative Stress, and Caspase-3 Activity.

Background and

Objectives

This study investigated the effects of oxytocin (OT) in a 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model in rats, focusing on its potential anti-inflammatory, antioxidant, and anti-apoptotic properties. Materials and

Methods

Forty male Wistar albino rats were randomly assigned to five groups (n = 8): control (intrarectal saline), TNBS-induced colitis, dexamethasone-treated colitis (1 mg/kg, i.p.), and two OT-treated colitis groups (0.5 and 1 mg/kg, i.p.). Body weight changes were recorded over 72 h. Macroscopic and histopathological evaluations were performed following laparotomy and colectomy. Serum and colon tissue samples were analyzed for TNF-α, IL-1β, IL-6, MPO, MDA, GSH, GPx, SOD, and CAT levels. Immunohistochemical analysis of caspase-3 and oxytocin receptor (OTR), as well as immunofluorescence-based OTR expression, were assessed.

Results

OT treatment significantly improved macroscopic and histopathological findings compared with the colitis group (p < 0.01). Tissue TNF-α and MDA levels were reduced, while antioxidant parameters were generally improved in OT-treated groups. Caspase-3 immunoreactivity decreased, indicating reduced apoptosis. Although some changes were observed in IL-6 levels, these were not consistent across all comparisons. OTR immunoreactivity appeared reduced in colitis and partially restored following OT administration.

Conclusions

OT attenuates experimental colitis by modulating inflammation, oxidative stress, and apoptosis, and may contribute to mucosal healing. These findings suggest that OT has potential as a supportive therapeutic agent in inflammatory bowel disease; however, further studies are required to clarify its mechanisms of action.