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In Vitro Protective Effects of a Standardized Extract of (L.) Mill. Cladodes and L. Leaves Against Indomethacin-Induced Intestinal Epithelial Cell Injury.
Antioxidants (Basel)
December 2024
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale F. Stagno D'Alcontres 31, 98166 Messina, Italy.
Nonsteroidal anti-inflammatory drugs (NSAIDs) can induce serious adverse effects in gastrointestinal (GI) mucosa, increasing intestinal permeability and leading to mitochondrial dysfunction, oxidative stress, apoptosis and inflammation. As proton pump inhibitors are effective in protecting against NSAID-induced gastropathy but not NSAID-induced enteropathy, current research is focused on natural products as protective substances for therapy and prevention of intestinal injury. Herein, through the use of an in vitro model based on intestinal epithelial cell (Caco-2) damage caused by indomethacin (INDO), we examined the protective activity of a commercially available standardized extract (OFI+OE) from (L.
View Article and Find Full Text PDFPhysicians' attitudes toward gastroprotective strategies for nonsteroidal anti-inflammatory drug prescription.
Proc (Bayl Univ Med Cent)
November 2024
Division of Gastroenterology and Hepatology, Case Western Reserve University, Cleveland, Ohio, USA.
Introduction: There is a paucity of information regarding providers' attitudes toward gastric-protective strategies with concurrent use of nonsteroidal anti-inflammatory drugs (NSAIDs). We aimed to assess gastric-protective strategies used upon prescribing NSAIDs and providers' awareness of societal guidelines for preventing NSAID-induced gastric complications.
Methods: A standardized 10-item questionnaire was sent to all orthopedic providers in North Carolina and South Carolina.
Activation of sirtuin 3 and maintenance of mitochondrial homeostasis by artemisinin protect against diclofenac-induced kidney injury in rats.
Naunyn Schmiedebergs Arch Pharmacol
November 2024
Clinical Pharmacology Department, Faculty of Medicine, Mansoura University, Mansoura, 31516, Egypt.
Nonsteroidal anti-inflammatory drug (NSAID)-induced kidney injury is one of the most common causes of renal failure. The exact pathogenesis of NSAID induced kidney injury is not fully known and the treatment is still challenging. Artemisinin (ART) gains more attention by its potent biological activities in addition to its antimalarial effect.
View Article and Find Full Text PDFGardenia jasminoides fruit extract alleviates non-steroidal anti-inflammatory drug-induced gastropathy in rats.
BMC Complement Med Ther
November 2024
Center of Excellence in Alternative and Complementary Medicine for Gastrointestinal and Liver Diseases, Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Background: NSAID-induced gastropathy is a health burden that requires effective intervention. Among various prevention options, Gardenia jasminoides fruit extract (GJE) has demonstrated gastroprotective effects through anti-inflammatory pathways with a wide safety margin. However, the detailed molecular mechanisms of GJE regarding mucoprotective and anti-inflammatory effects remained to be explored.
View Article and Find Full Text PDFEffect of tegoprazan, a novel potassium-competitive acid blocker, on non-steroidal anti-inflammatory drug (NSAID)-induced enteropathy.
Sci Rep
November 2024
Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Korea.
Article Synopsis
- The use of NSAIDs for chronic conditions has led to an increase in NSAID-induced enteropathy, creating a need for effective preventive and treatment strategies.
- Tegoprazan was tested on human epithelial cells exposed to indomethacin, showing a significant improvement in cell viability and restoration of tight-junction protein levels, which are crucial for intestinal health.
- The study concluded that tegoprazan protects small intestinal epithelial cells from NSAID-induced damage by enhancing tight junction protein expression and reducing inflammation and cell death.
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