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Modelling the Viscoelastic Pressure-Volume Curve of the GB
Published in Wenguang Li, Biliary Tract and Gallbladder Biomechanical Modelling with Physiological and Clinical Elements, 2021
Indomethacin is a NSAID blocking the production of prostaglandins which not only influence smooth muscle contractility but also relieve inflammation. Indomethacin can reduce or abolish GB smooth muscle spontaneous rhythmical contractions by inhibiting endogenous prostaglandin synthesis (Brotschi et al. 1984; Doggrell and Scott 1980; Kotwall et al. 1984). The other studies showed that indomethacin can improve GB emptying of patients with gallstones (O’Donnell et al. 1992) or animal models with cholecystitis (Yau et al. 1973) and has no effect on healthy GBs (Parkman et al. 2001; Murray et al. 1992). Based on those observations, it is concluded that the change in biomechanical property of GB smooth muscle is attributed to indomethacin.
Adsorption of Miscellaneous Organic Compounds from Nonaqueous Solutions
Published in Alexander Samokhvalov, Adsorption on Mesoporous Metal-Organic Frameworks in Solution for Clean Energy, Environment, and Healthcare, 2017
Indomethacin (Figure 11.4) is a nonsteroidal antiinflammatory drug (NSAID). The adsorption of indomethacin on several MIL-101 MOFs was studied (Čendak et al. 2014) from the solution in tetrahydrofuran (THF).
Thymol Reduces Hepatorenal Oxidative Stress, Inflammation and Caspase-3#xd; Activation in Rats Exposed to Indomethacin
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Tijani Abiola Stephanie, Olori O. David, Ebenezer O. Farombi
Drug-induced multi-organ toxicities are common adverse reaction triggered by numerous drugs like indomethacin (IND). Indomethacin is one of the non-steroidal anti-inflammatory drugs used as analgesic and also has antipyretic property. However, its adverse side effects have raised a lot of concern for its continuous use in clinical settings. Indomethacin cause many organ toxicities including liver, kidney and gastrointestinal toxicities in humans and experimental animals [1,2]. In the liver, IND has been associated with hepatocellular enzymes elevation and cholestatic jaundice whereas in the kidney, IND caused acute interstitial nephritis typified by wide spread interstitial edema with infiltration of inflammatory cells [3,4]. The mechanisms by which IND causes its toxicities include prostaglandin synthesis inhibition, generation of reactive oxygen species (ROS) resulting to cellular oxidative stress, inflammation and apoptosis [5].
Mechanisms underlying the healing potentials of the methanol extract of Chasmanthera dependens stem on indomethacin-induced gastric ulcer
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Abiola Stephanie Tijani, Ebenezer Olatunde Farombi, Samuel Babafemi Olaleye
Gastric ulcer is one of the leading chronic ailments of the gastrointestinal tract [1,2] caused by administration of nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol consumption, stress, Helicobacter pylori, smoking and nutritional deficiencies [3]. Untreated gastric ulcers may gradually deteriorate and result in unexpected complications, such as bleeding or perforation [4,5]. Indomethacin is a non-steroidal anti-inflammatory drug with antipyretic, antithrombotic and analgesic effects [6]. Its most common side effect is a gastrointestinal injury like gastric ulcers [7]. Mechanisms involved in indomethacin-induced gastric ulcer include inhibition of cyclooxygenase (COX), an enzyme responsible for prostaglandins synthesis, generation of free radicals, neutrophil infiltration, inhibition of angiogenesis and induction of apoptosis [8–12]. Prostaglandins are cytoprotective agents in the gastric mucosa, they stimulate the secretion of bicarbonate and mucus, maintain mucosal blood flow, and regulate mucosal cell turnover and repair [13]. Inhibition of prostaglandins synthesis, especially prostaglandin E2 (PGE2) by indomethacin and other members of the NSAIDs can slow down the healing process of gastric ulcers through their anti‑inflammatory activity [14].
Fabrication, controlled release, and kinetic studies of indomethacin—layered zinc hydroxide nanohybrid and its effect on the viability of HFFF2
Published in Journal of Dispersion Science and Technology, 2018
Behzad Soltani, Hafezeh Nabipour, Navid Ahmadi Nasab
Indomethacin (Figure 1) is a nonsteroidal anti-inflammatory drug that is widely used in treatment of trauma, osteoarthritis, rheumatoid arthritis, gouty arthritis, or enclosing spondylitis. It is an acidic hydrophobic drug that is practically insoluble in aqueous solutions with neutral or acidic pH, but is freely soluble in alkaline solutions.[22] Due to poor dissolution in the fluids of the gastrointestinal tract, this compound often shows low absorption and low erratic oral bioavailability. Additionally, undesirable physical properties may increase such as the irritation side effects on the gastrointestinal tract because of prolonged contact time with the mucosa.[23] Thus, rapid indomethacin absorption is desirable, to achieve the improvement of indomethacin solubility for its sustained release. In the present work, indomethacin as a model drug intercalated into LZH via an ion exchange approach. The controlled release behavior of the indomethacin-LZH nanohybrid has been studied in PBS solution at pH values of 4.8 and 7.4. Based on the results obtained in the controlled release behavior, the kinetic properties of the nanohybrid have been determined.