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Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) have been implemented in clinical settings for a long time for their anti-inflammatory effects. With the number of NSAID users increasing, gastroenterological physicians and researchers have worked hard to prevent and treat NSAID-induced gastric mucosal injury, an effort that has for the large part being successful. However, the struggle against NSAID-induced mucosal damage has taken on a new urgency due to the discovery of NSAID-induced small intestinal mucosal injury. Although the main mechanism by which NSAIDs induce small intestinal mucosal injury has been thought to depend on the inhibitory effect of NSAIDs on cyclooxygenase (COX) activity, recent studies have revealed the importance of mitochondria-derived reactive oxygen species (ROS) production, which occurs independently of COX-inhibition. ROS production is an especially important factor in the increase of small intestinal epithelial cell permeability, an early stage in the process of small intestinal mucosal injury. By clarifying the precise mechanism, together with its clinical features using novel endoscopy, effective strategies for preventing NSAID-induced small intestinal damage, especially targeting mitochondria-derived ROS production, may be developed.
Acknowledgements
This work was supported by Grants-in-Aid for Scientific Research © to Y.N. (No.25460958) from the Japan Society for the Promotion of Science, and by an Adaptable and Seamless Technology Transfer Program through target-driven R&D to Y.N. from the Japan Science and Technology Agency.
Declaration of interest
The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.
Y.N. received scholarship funds from Otsuka Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., and Eisai Co., Ltd.