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Peer-reviewed veterinary case report

Citral impairs intestinal changes caused by ulcerative colitis through modulation of antioxidant, anti-inflammatory and healing activities.

Journal:
Inflammopharmacology
Year:
2026
Authors:
Emílio-Silva, Maycon T et al.
Affiliation:
Department of Structural and Functional Biology · Brazil
Species:
rodent

Abstract

INTRODUCTION: Ulcerative colitis (UC) is the main representative of inflammatory bowel diseases (IBD) are chronic conditions characterized by intestinal inflammation, caused by the overproduction of pro-oxidant species and an immune response that damages the gut mucosa. OBJECTIVE: To evaluate the anti-inflammatory and protective effect of Citral, a monoterpene, on in vitro and in vivo models of UC. METHODOLOGY: Male C57BL/6J mice were used for DSS 3%-induced UC for 5 days in drinking water. Concomitantly, daily oral citral (25, 100, and 300&#xa0;mg/kg, p.o.) or vehicle was administered. Colonic segments were collected to evaluate neutrophil infiltration, lipid peroxidation, and the expression of antioxidant markers. NCM-356 and RAW-294 cells were stimulated with LPS (10 and 100 ng/mL, respectively). Cell viability, nitrite levels, scratch wound healing assay, and gene expression of inflammatory and growth factors were assessed. RESULTS: Acute treatment with citral (100 and 300&#xa0;mg/kg) exhibited an anti-colitis effect by reducing the disease activity index (DAI) score compared to that in the DSS-vehicle group. This response was mediated by a significant reduction in myeloperoxidase activity and thiobarbituric acid reactive species levels, associated with an increase in superoxide dismutase activity, indicating anti-inflammatory and antioxidant activities (p&#x2009;<&#x2009;0.05). The monoterpene reversed LPS-induced intestinal epithelial disturbance in the scratch wound healing process under different conditions and possibly reduced inos expression. CONCLUSION: Citral treatment prevents the development of UC via anti-inflammatory, antioxidant, and healing effects.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/41335164/