Etiopathogenesis of Peptic Ulcers and Prostaglandin Relationship

Laurus nobilis Esansiyel Yağının Sıçanlarda İndometasin Kaynaklı Mide Ülserinin Azaltılmasında Potansiyel Rolü

“…Indeed, in our study, we observed that INDO administration significantly down-regulated nitric oxide levels, which aligns with the suppression of endogenous prostaglandin production. [21][22][23] This finding mirrors the literature, where reduced NO availability is closely associated with increased gastric vulnerability and ulceration. 21,24 Our findings indicate LANO application may counteract indomethacin's negative effects, supporting gastric protection via the NO pathway.…”

“…This aligns with previous studies that have established the role of oxidants in developing NSAID-induced gastric ulcers. 22,28 LANO showed promising effects with diverse phytochemicals. It displayed significant antioxidant, anti-diabetic, and antimicrobial effects at low concentrations, therapeutic potential.…”

Evaluation of anti-gastric ulcer activity of aqueous and 80% methanol leaf extracts of Urtica simensis in rats

“…Ethanol is readily penetrates the gastric mucosa due to its ability to solubilize the protective mucous and expose the mucosa to the proteolytic and hydrolytic actions of hydrochloric acid and pepsin [ 5 ] and also cause profound micro-vascular changes with strong vasoconstriction accompanied by arteriolar dilatation responsible for engorgement of mucosal capillaries [ 8 ]. The pathogenesis of mucosal damage in the stomach is associated with reduction of bicarbonates secretion and generation of ROS that seem to play a vital role in the formation of lipid peroxides, accompanied by impairment of anti-oxidative enzyme activity of cells [ 32 ].…”

“…In pylorus-ligated-induced peptic ulcers ligation of the pyloric end of the stomach causes accumulation of gastric acid in the stomach that produces ulcers and important to measure acidic content [ 7 ]. NSAID and ethanol induced ulcers are important in examining the potential usefulness of anti-secretory and cytoprotective agents since the fundamental pathophysiology involves gastric acid secretion and mucosal prostaglandin synthesis [ 8 ].…”