Related Experiment Video
Updated: Aug 9, 2026
07:50
Facilitating Drug Discovery: An Automated High-content Inflammation Assay in Zebrafish
Published on: July 16, 2012
NO-NSAIDs: from inflammatory mediators to clinical readouts
Stefano Fiorucci1, Elisabetta Antonelli
1University of Perugia, Italy. fiorucci@unipg.it
Inflammation & Allergy Drug Targets
|April 15, 2006
Summary
New nitric oxide-releasing non-steroidal anti-inflammatory drugs (NO-NSAIDs) offer reduced side effects. These innovative anti-inflammatory drugs combine NSAID efficacy with nitric oxide (NO) release for improved safety profiles.
Area of Science:
- Pharmacology
- Drug Development
Background:
- Non-steroidal anti-inflammatory drugs (NSAIDs) and COX-2 inhibitors (COXIBs) are widely used but associated with significant gastrointestinal, cardiovascular, and renal side effects.
- Nitric oxide (NO)-releasing NSAIDs (NO-NSAIDs) represent a novel therapeutic class designed to mitigate these adverse effects.
Purpose of the Study:
- To evaluate the safety and efficacy profile of NO-NSAIDs, particularly nitroxybutyl-NO-NSAIDs.
- To investigate the mechanism by which NO release may counteract NSAID-induced toxicity.
Main Methods:
- Extensive human studies on nitroxybutyl-NO-NSAIDs.
- Pre-clinical investigations into the pharmacological actions of NO-NSAIDs.
Main Results:
- Nitroxybutyl-NO-NSAIDs demonstrate balanced inhibition of COX isoforms and release nitric oxide (NO).
- NO-NSAIDs exhibit reduced gastrointestinal and cardiorenal toxicity compared to traditional NSAIDs.
- Clinical trial data align with pre-clinical findings, supporting the safety profile of NO-NSAIDs.
Conclusions:
- NO-NSAIDs offer a promising alternative to conventional NSAIDs, with a favorable safety profile due to integrated nitric oxide release.
- The NO released from NO-NSAIDs may counteract NSAID-induced gastric mucosal damage, contributing to reduced gastrointestinal toxicity.
Related Concept Videos
01:29Inflammatory Bowel Disease IV: Pharmacological Management
Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Pharmacologic...
01:29Drugs for Treatment of Ulcerative Colitis in IBD
Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation.
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
01:25Acute Inflammation III: Local and Systemic Effects
Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
02:26NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
01:26Acute Inflammation I: Inflammatory Response
Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...