Abstract

With the wide application of non-steroidal anti-inflammatory drugs (NSAIDs), their gastrointestinal side effects are an urgent health burden. There are currently sound preventive measures for upper gastrointestinal injury, however, there is a lack of effective defense against lower gastrointestinal damage. According to a large number of previous animal experiments, a variety of NSAIDs have been demonstrated to induce small intestinal mucosal injury in vivo. This article reviews the descriptive data on the administration dose, administration method, mucosal injury site, and morphological characteristics of inflammatory sites of various NSAIDs. The cells, cytokines, receptors and ligands, pathways, enzyme inhibition, bacteria, enterohepatic circulation, oxidative stress, and other potential pathogenic factors involved in NSAID-associated enteropathy are also reviewed. We point out the limitations of drug modeling at this stage and are also pleased to discover the application prospects of chemically modified NSAIDs, dietary therapy, and many natural products against intestinal mucosal injury.

Highlights

  • Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used drugs worldwide (Scarpignato and Hunt, 2010)

  • 3.3.1 Hepatobiliary Excretion of NSAIDs NSAID-induced intestinal epithelial damage is due to direct effects after oral administration, recurrent local effects are due to enterohepatic recirculation of the drug, and systemic effects occur after absorption (Lanas and Sopena, 2009)

  • Enteritis involved in numerous experiments is a simple model of acute NSAIDassociated injury rather than chronic inflammation

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Summary

INTRODUCTION

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used drugs worldwide (Scarpignato and Hunt, 2010). Their most common side effects are gastric and intestinal mucosal damage. Attention was focused only on preventing gastric complications. The occurrence of NSAID-associated enteropathy has received increasing attention, especially after the advent of enteric-coated preparations of NSAIDs. Data have reported that severe damage to the small intestine accounts for one-third of NSAID complications (Scarpignato and Hunt, 2010). With the aging population in China, the use of NSAIDs will continue to increase, and conquering the side effects of small intestinal injury has gradually become a clinical problem. Treatment and preventive measures need to be taken as soon as possible

Indomethacin
Diclofenac
Aspirin
Flurbiprofen
Naproxen
Loxoprofen
Ibuprofen
Diflunisal
2.10 Paracetamol
2.11 Ketoprofen
COX Inhibition
Uncoupling of Mitochondrial Oxidative Phosphorylation and Oxidative Stress
Hepatobiliary
Bile Acid Receptors
Bacteria and Bacterial Components
Toll-like Receptor 4
Innate Immune Cells Monocytes are involved in the development of inflammation
Cytokines/Enzymes/Receptors in
Food Intake
Autophagy Inhibition
Psychological States
3.10 Drug Interaction
Findings
CONCLUSION
Full Text
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