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Updated: Jul 12, 2025

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
Published on: February 27, 2014
Virgin Coconut Oil Alleviates Dextran Sulphate-Induced Inflammatory Bowel Disease and Modulates Inflammation and
Silpa Prabha1, Sanjay Tamoli2, Achuthan C Raghavamenon3
1Department of Immunology, Amala Cancer Research Centre, Amala Nagar, Thrissur, India.
Objective:
Virgin coconut oil (VCNO), an unrefined kernel oil from Cocos nucifera L., has considerable medicinal and nutritive value. Experimental evidence suggests its antioxidant, anti-inflammatory, chemoprotective, analgesic, and hypolipidemic effects. Presently, the effect of VCNO on ameliorating dextran sodium sulfate (DSS)-induced inflammatory bowel disease and cyclophosphamide (CTX)-induced immunosuppression in experimental animals was analyzed.
Method:
DSS (4%) was administered to BALB/c mice through drinking water for 12 days to induce inflammatory bowel disease, and VCNO (500, 750, and 1000 mg/kg bwt) was supplemented orally for 12 days. For anti-inflammatory studies, lipopolysaccharide (LPS, 250 µg/animal) was injected into the intraperitoneal cavity of Swiss albino mice followed by 7 days' pretreatment of VCNO (500, 750, and 1000 mg/kg bwt). To understand the mechanism of action, serum from all animals was collected after 6 hours of LPS challenge and levels of proinflammatory cytokines were analyzed using enzyme-inked immunosorbent assay. In addition to this, immunosuppression was induced by CTX (50 mg/kg bwt, po) in Swiss albino mice.
Results:
Oral administration of VCNO effectively reversed the pathologies associated with inflammatory bowel disease induced by DSS, including loss of body weight, increased disease activity index, shortening of colon length, diarrhea, and rectal bleeding. Histopathological examination showed that VCNO restored the damage in colon tissue induced by DSS. Similar trends were noticed in levels of myeloperoxidase and mRNA expression of proinflammatory cytokines in colon tissue. In addition to this, supplementation of VCNO markedly reduced the hike in the level of serum proinflammatory cytokines in LPS-challenged mice. Further, administration of VCNO effectively increased spleen and thymus indexes and stimulated the production of interferon-γ in serum.
Conclusions:
Overall, this study revealed that VCNO alleviates inflammatory bowel disease and inflammation; concurrently, it can revert immunosuppression.
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