This study was conducted to assess the feasibility of COX1 NSAID substitution for aspirin for preventative therapy related to circulating anticoagulants, as manifest by inhibition of platelet aggregation. There was no difference in platelet aggregation inhibition between aspirin, naproxen, ketoprofen or diclofenac and misoprostol (in combination in the form of Arthrotec). As COX1 NSAIDs appear equivalent in platelet inhibition efficacy to aspirin, therapeutic regimens can be simplified in those individuals who require an NSAID for other problems. Further, despite its short serum halflife, Arthrotec appears as effective as an antiplatelet agent. Controlled, double blind studies of efficacy in blocking clinical events (both cardiovascular and gastrointestinal) are recommended.
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http://dx.doi.org/10.4081/reumatismo.2004.89 | DOI Listing |
Vet Med Sci
January 2025
Department of Medical Pharmacology, Faculty of Medicine, Ataturk University, Erzurum, Turkey.
The present study aimed to unveil the gastroprotective potential of Vaccinium macrocarpon (VM) extract and its mechanism of action against indomethacin (INDO)-induced gastric ulcers in rats. To achieve this goal, rats were pretreated with either omeprazole (20 mg/kg) or VM (100 mg/kg) orally for 14 consecutive days. Gastric tissue samples were collected and various parameters were evaluated to understand the mechanism of VM's action, including the levels of superoxide dismutase, malondialdehyde, glutathione, CAT and transforming growth factor beta (TGF-β), as well as the mRNA expression levels of tumour necrosis factor alpha, interleukin 1 beta, nuclear factor kappa B (NF-κB) and inhibitor kappa B (IκB).
View Article and Find Full Text PDFNon-steroidal anti-inflammatory drugs (NSAIDs) are popular choices for the mitigation of pain and inflammation; however, they are accompanied by side effects in the gastrointestinal and cardiovascular systems. We compared the effects of naproxen, a traditional NSAID, and celecoxib, a cyclooxygenase - 2 (Cox-2) inhibitor, in humans. Our findings showed a decrease in tryptophan and kynurenine levels in plasma of volunteers treated with naproxen.
View Article and Find Full Text PDFPain Ther
December 2024
Department of Anesthesiology and Pain Medicine, Dokkyo Medical University School of Medicine, Tochigi, Japan.
Introduction: Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for pain disorders and exert pharmacological effects by inhibiting cyclooxygenase (COX). Although previous studies have evaluated the COX inhibitory activity and selectivity of NSAIDs, none has compared COX inhibitory concentrations with the plasma concentrations of clinical doses or investigated the efficacy and adverse effects of different dosage forms. Therefore, in this study we evaluated the COX inhibitory activities and inhibition rates of clinical doses of the various NSAID formulations, especially diclofenac sodium.
View Article and Find Full Text PDFJ Clin Med
December 2024
Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, 08907 Barcelona, Spain.
In patients with aspirin-exacerbated respiratory disease (AERD), there is disparate regulation of prostaglandin E2 (PGE) and prostaglandin D (PGD). Both prostanoids are synthesised by cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2). However, while the basal synthesis of PGE tends to decrease, that of PGD increases in patients with AERD.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Chemistry and Mineralogy, Institute of Bioanalytical Chemistry, Leipzig University, Deutscher Platz 5, 04103, Leipzig, Germany.
In this study, we investigated a novel anti-cancer drug design approach by revisiting diclofenac-based carborane-substituted prodrugs. The redesigned compounds combine the robust carborane scaffold with the oxindole framework, resulting in four carborane-derivatized oxindoles and a unique zwitterionic amidine featuring a nido-cluster. We tested the anti-cancer potential of these prodrugs against murine colon adenocarcinoma (MC38), human colorectal carcinoma (HCT116), and human colorectal adenocarcinoma (HT29).
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