Keskin,I˙.Alkan,I.Keskin,M.Kaplan,S.2024-10-152024-10-1520210978-153619215-5978-153619128-8[SCOPUS-DOI-BELIRLENECEK-18]2-s2.0-85152416107https://hdl.handle.net/20.500.14517/6861Non-steroidal anti-inflammatory drugs (NSAIDs) are frequently employed for the treatment of pain, fever, and inflammation. Diclofenac sodium (DS) exhibits potent anti-inflammatory, analgesic, and antipyretic effects. Studies have investigated DS neurotoxicity, especially in the first trimester of pregnancy. Studies of the impacts of prenatal DS exposure on the nervous system show that DS exhibits neurotoxic effects in the pyramidal and granular cells of the hippocampus and in the Purkinje cells of the cerebellum. Although some information is available concerning the teratogenic effects of DS on the nervous system, less is known regarding the effect of DS use on the development of the peripheral nervous system. Oxidative stress generated by DS through the enzyme cyclooxygenase can disrupt the integrity of the nervous system, including its myelin and axon content, and thus cause developmental problems in embryonic life. Melatonin may be used as a neuroprotective agent to reduce the neurotoxic effect of DS on nervous system development. However, the mechanism involved in the neuroprotective activity of melatonin in the development of the nervous system has not been entirely elucidated. This chapter describes the neuroprotective effect and mechanism of melatonin against DS toxicity. © 2021 by Nova Science Publishers, Inc. All rights reserved.eninfo:eu-repo/semantics/closedAccessMelatoninNeurotoxicityNon-steroidal anti-inflammatory drugsPeripheral nervous system developmentBook Part389405