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Updated: Aug 25, 2026

Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
Published on: February 16, 2022
Nitric oxide: potential role for reducing gastro-enteropathy
Matthew Walley1, Christoph Hotz-Behofsits, Robert Simpson
1Department of Medicine, Guys, Kings and St Thomas' School of Medicine, Bessemer Road, London SE5 9PJ, UK. matthew.walley@kcl.ac.uk
Abstract:
The pathogenesis of non-steroidal anti-inflammatory drug (NSAID)-induced gastroenteropathy may involve a number of key events leading to increased intestinal permeability and inflammation (topical effect) and the development of ulcers (micro-vascular effects of COX-1 inhibition and prostaglandin deficiency). Many strategies have been employed in an attempt to reduce the toxic effects of NSAIDs and these have been targeted at the different pathogenic stages of lesion development. One of the latest in this long chain of damage limitation has been the development of nitric oxide (NO) sequestering NSAIDs (NO-NSAIDs). It is suggested that the NO, which is released as the compounds are broken down, may counteract the consequences of the NSAID-induced decrease in mucosal prostaglandins. Here we examine the proposed mechanisms for NSAID-induced gastrointestinal damage together with some of the methods employed to address these mechanisms. We also consider the physiologic roles of NO in the gut together with how it may be potentially employed as an agent for limiting the side effects of NSAIDs in the gastrointestinal tract.
Insights
Non-steroidal anti-inflammatory drug (NSAID)-induced gastroenteropathy involves increased intestinal permeability and ulcers. Nitric oxide-releasing NSAIDs (NO-NSAIDs) may counteract these damaging effects by releasing nitric oxide (NO).
Area of Science:
- Gastroenterology
- Pharmacology
- Drug Development
Background:
- Non-steroidal anti-inflammatory drugs (NSAIDs) can cause significant gastrointestinal damage, including increased intestinal permeability, inflammation, and ulcer formation.
- These effects are attributed to topical injury and micro-vascular changes resulting from cyclooxygenase-1 (COX-1) inhibition and prostaglandin deficiency.
Purpose of the Study:
- To examine the mechanisms underlying NSAID-induced gastrointestinal damage.
- To review strategies developed to mitigate NSAID toxicity.
- To explore the potential of nitric oxide (NO) and NO-releasing NSAIDs (NO-NSAIDs) in preventing NSAID-induced gastroenteropathy.
Main Methods:
- Review of proposed pathogenic mechanisms of NSAID-induced gastroenteropathy.
- Analysis of various strategies employed to reduce NSAID toxicity.
- Examination of the physiological roles of nitric oxide (NO) in the gastrointestinal tract.
Main Results:
- NSAID-induced gastroenteropathy involves topical effects and micro-vascular changes.
- Nitric oxide (NO) plays a physiological role in the gut.
- Nitric oxide-releasing NSAIDs (NO-NSAIDs) are a novel strategy to counteract NSAID-induced mucosal damage.
Conclusions:
- NSAID-induced gastrointestinal damage is multifactorial.
- Nitric oxide (NO) may serve as a protective agent against NSAID toxicity.
- NO-NSAIDs represent a promising therapeutic approach to limit NSAID-related gastrointestinal side effects.
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