Gastroprotective and ulcer healing effects of nitric oxide-releasing non-steroidal anti-inflammatory drugs
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2017, Biomedicine and PharmacotherapyCitation Excerpt :The suppression of ROS (reactive oxygen species) is responsible for gastroprotection against gastric acute lesions induced by 3.5 h of WRS (water immersion restraint). These analogues cause an attenuation of lipid peroxidation, decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by increase of SOD activity [186]. Novel dihydroartemisinin-nitric oxide donor hybrid based derivatives such as compound 49 have been designed and synthesized as multitarget agents.
The nitric oxide donor cis-[Ru(bpy)<inf>2</inf>(SO<inf>3</inf>)NO](PF<inf>6</inf>) increases gastric mucosa protection in mice - Involvement of the soluble guanylate cyclase/K<inf>ATP</inf> pathway
2015, Nitric Oxide - Biology and ChemistryCitation Excerpt :We demonstrated that inhibition of soluble guanylate cyclase completely abolished the protective effect of FOR0810 in two models of gastric damage. Our results are compatible with those obtained by Brzozowski et al. [34], who found that ODQ treatment completely abolished the protective effect of NO-releasing NSAIDs against ethanol-induced gastric damage. The participation of KATP channels in several models of gastric protection was previously described [4,9,35].
NO-donating NSAIDs and cancer: An overview with a note on whether NO is required for their action
2008, Nitric Oxide - Biology and ChemistryGaseous Mediators as a Key Molecular Targets for the Development of Gastrointestinal-Safe Anti-Inflammatory Pharmacology
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