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Gastric ulcers resulting from the continuous use of NSAIDs may be related to mechanisms that include a local damaging action for destabilizing the membrane phospho-lipid layer and damaging the mucus barrier, favouring the retro-diffusion of H + ions that damage the surface cells of the gastric mucosa, inhibition of the enzyme cyclo-oxygenase (COX) and consequently the reduction of the synthesis of cytoprotective prostaglandins (PGE2 and PGI2), which act by stimulating the production of mucus and bicarbonate, in maintaining blood flow and in the negative regulation of gastric acid secretion (Rocha Caldas et al., 2015), thymol (Ribeiro et al., 2016
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