[2] Especially, NSAID use is associated with increased risk of developing toxicity not only in the upper but also in the lower GI tract.[3] The long-term uses of NSAID have side-effects such as GI mucosal injury, and serious complications can lead to mortality in some elderly

MG-132 patients.[4] The severity of gastric mucosal injury by NSAIDs is associated with the loss of mucosal integrity, gastric mucosal bleeding, reduction in inherent anti-oxidant defense of gastric mucosa, apoptosis of mucosal cells, inhibition of cell renewal, and migration of cells of gastric pits to the damaged epithelial lining.[5, 6] Therefore, vigorous efforts are being done in discovering safer NSAID molecules capable of inhibiting the synthesis of pro-inflammatory lipid mediators to reduce the side-effects associated

with long-term therapies. Because gastric mucosal damages are a common adverse effect of traditional NSAIDs, patients at risk should receive prevention therapies. Current prevention PD0332991 supplier strategies in patients who need NSAIDs should also take into account the presence of cardiovascular risk factors, as selective COX-2 inhibitors (coxibs) and probably most traditional NSAIDs increase the incidence of serious cardiovascular events. Patients without risk factors should be treated with traditional NSAIDs, whereas patients at risk may receive co-therapy with a proton pump inhibitor (PPI) or misoprostol, or a coxib alone.[7] Patients with risk factors requiring anti-inflammatory drugs may be prescribed a gastroprotectant such as misoprostol, or anti-secretory agents. Selective coxibs, such as celecoxib, became popular because they are as effective as conventional agents in reducing pain and improving physical functioning in people with arthritis, and are associated with fewer gastric adverse events. In addition to selected pharmacological

agents, botanical and medicinal plant extracts are also being investigated. Indomethacin is an indol derivative, NSAID with anti-inflammatory, selleck chemical analgesic, and antipyretic effects. Indomethacin became the first-choice drug to produce an experimental ulcer model as a result of having a higher ulcerogenic potential than other NSAIDs.[8] There have been several reports about the ulcerogenic mechanism of indomethacin. It has been suggested that indomethacin induces gastric damage via inhibiting the release of protective factors like COX-1, prostaglandin E2 (PGE2), bicarbonate, and mucus, accompanied with increasing aggressive factors like acid and increasing oxidant parameters while decreasing anti-oxidant parameters. Therefore, indomethacin-induced gastric damage model as potent inducer of gastric ulcer is frequently used to study the antiulcer activity of certain drugs. Garlic is one of the oldest medicinal plants and is well recognized for its diverse health benefits. Raw garlic has a relatively low bioactive material content.