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Gastrointestinal Function and Toxicology in Canines
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
Sucralfate is an oral antiulcer agent that acts by forming a protective barrier over the site of an ulcer and is a complex of sucrose octasulfate and polyaluminum hydroxide. It the local environment of the stomach, polymerization and cross-linking occur, which results in the formation of a sticky, yellow-white gel that combines with proteinaceous exudates in the stomach to form an adherent barrier preventing the contact of gastric acid with the lesion compromising the integrity of the mucosal barrier. However, continued exposure can result in the slow release of aluminum into the system and the development of constipation by a mechanism that is unclear.
Development of rebamipide-loaded spray-dried microsphere using distilled water and meglumine: physicochemical characterization and pharmacokinetics in rats
Published in Pharmaceutical Development and Technology, 2021
Dae Woong Ko, Jung Hyun Cho, Han-Gon Choi
Rebamipide [2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinon-4-yl] propionic acid], an amino acid derivative of 2-(1H)-quinolinone, has been used as a potent antiulcer agent, because it increases endogenous prostaglandin synthesis and scavenges oxygen-derived free radicals in damaged gastric mucosal cells (Holland et al. 2019; Jaafar et al. 2018; Simsek et al. 2019). It is a BCS (Biopharmaceutics Classification System) class IV drug, because of its low solubility and permeability (Ha et al. 2017; Takeuchi et al. 2018). In particular, rebamipide has been reported to provide absolute oral bioavailability of 4.8% in rats (Shi et al. 2013). Therefore, the solubility and permeability of oral rebamipide in the gastrointestinal tract are two factors in its enhanced oral bioavailability. Much research has been focused on its enhanced bioavailability resulting from increased permeability with penetration enhancers (Huang et al. 2008; Mustapha, Din, et al. 2016; Narala et al. 2019; Tanaka et al. 2019). However, the use of specific penetration enhancers has not been approved by the US FDA since these materials might induce severe irritation to biological membranes. Many solubility-enhancing techniques, such as solid dispersion (Pradhan et al. 2015; Xiong et al. 2017; Takeuchi et al. 2018; Tanaka et al. 2019), nanosuspension (Shi et al. 2013), orally disintegrating tablets (Takano et al. 2019) and nano/microemulsion (Kim et al. 2017; Narala et al. 2019), have been studied.
Teprenone for the prevention of low-dose aspirin-induced gastric mucosal injury in Helicobacter pylori-negative patients
Published in Scandinavian Journal of Gastroenterology, 2019
Taned Chitapanarux, Nirush Lertprasertsuke, Acharaporn Kongnak
The pathogenesis of gastrointestinal damage caused by aspirin related to its capability of lowering gastric prostaglandin levels by COX-1 inhibition [14]. Inhibition of prostaglandin synthesis reduces mucosal defenses, including mucus and bicarbonate secretion, blood flow, epithelial cell turnover and repair, and mucosal immunocyte function. Teprenone, a mucoprotective drug that promotes the endogenous synthesis of prostaglandins can serve as a broad-spectrum antiulcer agent and has a remarkable ability to repair and restore gastric mucosal integrity by slowing down the rate of its erosion and by stimulating mucus elaboration. Although, LDA reduced COX-1 expression in both groups of patients. The change of COX-1 IRS was significantly higher in placebo group than in teprenone group. The clinical dose of teprenone enhanced the gastric mucosal COX-1 expression that was inhibited by LDA. From these findings, it is possible that teprenone may prevent aspirin-induced gastric mucosal injury via stimulation of prostaglandin production by increasing COX expression.
In vivo anti-ulcerogenic effect of okra (Abelmoschus esculentus) on ethanol-induced acute gastric mucosal lesions
Published in Pharmaceutical Biology, 2018
Deniz Ortaç, Mustafa Cemek, Turan Karaca, Mehmet E. Büyükokuroğlu, Zafer Ö. Özdemir, Ayşe Tuba Kocaman, Sadık Göneş
The biochemical and histopathological results of the present study indicate that okra has potent gastroprotective effects against ethanol-induced gastric ulcer. Okra reduced the gastric injuries, lipid peroxidation, ulcerated area, edema, hemorrhage, cell infiltration, epithelial cell loss and improved antioxidant defense systems. We suggest that okra may be a useful therapeutic antiulcer agent.