Virgin coconut oil lessens trichloroacetic acid assault on the stomach and intestine of rats via enhancement of Nrf2 but inhibition of TNF-α, IL1β/NF-kB signalling pathway

Trichloroacetic acid (TCA), a known environmental toxicant, causes organ damage via oxidative stress and activation of pro-inflammatory cytokines. Virgin coconut oil (VCO) is known for many beneficial health effects associated with its phenolic acids and flavonoid contents. We, therefore, explore the mechanisms underlying the antioxidative and anti-inflammatory mechanisms of Virgin Coconut oil (VCO) alone, or combined with 5-fluorouracil (5FU) in the treatment of TCA-induced gastric and intestinal damage in rats. Rats received TCA (250 mg/Kg b.wt, p.o) for ten days, followed by either 5 % or 10 % VCO per gram feed alone or in combination with 5FU (50 mg/kg, i.p) for another ten days. Stomach and intestinal tissue oxidative stress parameters and inflammatory markers were evaluated along with histological examination. TCA's intoxication which caused a decrease in the activity of SOD, CAT, GPx, and Nrf2 in the stomach and colon, and an increase in MDA, MPO, TNF-α, IL-1β, and NF-kB levels were all reversed by VCO, either alone or in combination with 5-FU. Further, histomorphometry data favored the anti-inflammatory potentials of VCO. Parietal cell mass and inflammatory cell infiltration elaborated by TCA were reduced significantly by VCO and 5-FU. Similarly, intestinal crypt depth assessment and inflammatory cell infiltration earlier increased in the TCA group was quashed by VCO. Still, both gastric mucous and goblet cells hitherto reduced were significantly enhanced by VCO alone or in combination with 5-FU. Focal disruption of the gastric pit, derangement of surface epithelium, and sloughing of the surface epithelial barrier of the intestinal villi occasioned by TCA were all assuaged by VCO. Virgin coconut oil shows a promising adjunctive effect quashing trichloroacetic acid-induced injury in the stomach and intestine via suppression of lipid peroxidation, enhancement of Nrf2 but inhibition of TNF-α, IL-1β/NF-kB signaling.