Conclusions
Virgin coconut oil shows a possible association with antioxidant properties to control the regulation of prostaglandin synthesis and protect against reactive oxygen species damage.
Material and methods
Three groups of rats (6 rats per group for each ulcer model) were pre-treated with distilled water for the negative control group, 30 mg/kg of omeprazole for the positive control group and VCO (2 ml per rat) for the treatment group. Animals were pre-treated for 7 days and ulcers were induced with cold restraint stress, piroxicam, ethanol and pylorus ligation. On day eight, animals were sacrificed and ulcer scores were determined based on macroscopic evaluation. The gastric volume, pH, total acidity and mucus content were measured in the pylorus-ligated model. The levels of antioxidants were determined from the gastric tissue homogenates.
Methods
Three groups of rats (6 rats per group for each ulcer model) were pre-treated with distilled water for the negative control group, 30 mg/kg of omeprazole for the positive control group and VCO (2 ml per rat) for the treatment group. Animals were pre-treated for 7 days and ulcers were induced with cold restraint stress, piroxicam, ethanol and pylorus ligation. On day eight, animals were sacrificed and ulcer scores were determined based on macroscopic evaluation. The gastric volume, pH, total acidity and mucus content were measured in the pylorus-ligated model. The levels of antioxidants were determined from the gastric tissue homogenates.
Results
Virgin coconut oil significantly (p < 0.001) inhibited the ulceration caused by different inducers. The percentage of inhibition for the VCO-treated group was 78.3%, 84.7%, 72.7% and 73.1%, while for the omeprazole-treated group it was 60.8%, 61.5%, 59% and 53.8% in cold restraint stress, ethanol, piroxicam and pylorus-ligated ulcer models, respectively. Virgin coconut oil significantly (p < 0.001) inhibited gastric juice volume and total acidity for VCO and omeprazole treated groups as compared to the non-treated negative control group. Moreover, VCO and omeprazole caused a significant (p < 0.001) increase of gastric mucus content and pH. Virgin coconut oil also proved to have significantly increased glutathione (GSH) and nitrite levels, whereas the levels of SOD, GP, MDA and CAT were significantly (p < 0.001) reduced by VCO relative to the control group. Virgin coconut oil also significantly (p < 0.001) increased the level of prostaglandin in rat tissue homogenate, similar to the omeprazole treated group. Conclusions: Virgin coconut oil shows a possible association with antioxidant properties to control the regulation of prostaglandin synthesis and protect against reactive oxygen species damage.