Melatonin and multiple sclerosis: antioxidant, anti-inflammatory and immunomodulator mechanism of action

Abstract

Background Melatonin is an indole hormone secreted primarily by the pineal gland that showing anti-oxidant, anti-inflammatory and anti-apoptotic capacity. It can play an important role in the pathophysiological mechanisms of various diseases. In this regard, different studies have shown that there is a relationship between Melatonin and Multiple Sclerosis (MS). MS is a chronic immune-mediated disease of the Central Nervous System. Aim The objective of this review was to evaluate the mechanisms of action of melatonin on oxidative stress, inflammation and intestinal dysbiosis caused by MS, as well as its interaction with different hormones and factors that can influence the pathophysiology of the disease. Results Melatonin causes a significant increase in the levels of catalase, superoxide dismutase, glutathione peroxidase, glutathione and can counteract and inhibit the effects of the NLRP3 inflammasome, which would also be beneficial during SARS-CoV-2 infection. In addition, melatonin increases antimicrobial peptides, especially Reg3β, which could be useful in controlling the microbiota. Conclusion Melatonin could exert a beneficial effect in people suffering from MS, running as a promising candidate for the treatment of this disease. However, more research in human is needed to help understand the possible interaction between melatonin and certain sex hormones, such as estrogens, to know the potential therapeutic efficacy in both men and women.

Pretreatment of the ROS Inhibitor Phenyl-N-tert-butylnitrone Alleviates Sleep Deprivation-Induced Hyperalgesia by Suppressing Microglia Activation and NLRP3 Inflammasome Activity in the Spinal Dorsal Cord

“…Previous studies revealed that excessive ROS generation is associated with endoplasmic reticulum (ER) stress, which induces inflammatory response by activating the nuclear factor-kappa B (NF-κB) signaling pathway [34]. Oxidative stress is involved in the activation of NLRP3 inflammatory corpuscles, which is an important component of innate immunity involved in the process of inflammatory diseases of the CNS [35][36][37]. Latest studies have shown that NLRP3 is up-regulated in both neuropathic and inflammatory pain models, the activation of which, is also involved in the occurrence and maintenance of postoperative pain [38].…”

Is Melatonin the “Next Vitamin D”?: A Review of Emerging Science, Clinical Uses, Safety, and Dietary Supplements

“…Promising, emerging research indicates that melatonin supplementation may have therapeutic benefits for autoimmune conditions, such as multiple sclerosis (MS) and perhaps Hashimoto’s thyroiditis, most likely due to its involvement in anti-inflammatory mechanisms, oxidative stress reduction, and modulation of the gut microbiota [ 165 ]. Melatonin is linked to the seasonal relapse rate in patients with MS [ 166 ].…”

“…Glutathione is one of the major antioxidant systems in the body and is susceptible to changes in redox status and nutrient supply [ 315 ]. Various research studies have confirmed that there are individual associations between melatonin and glutathione [ 165 ], and glutathione and vitamin D [ 316 ]. Thus, while not yet extensively researched, there could be an interrelationship between the collective antioxidant activities of glutathione, vitamin D, and melatonin.…”

Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice

“…Melatonin 10.3389/fncel.2023 synthesis undergoes changes with age and in experimental demyelination (Hardeland, 2012;Wurtman, 2017). In contrast, the exogenous melatonin exhibits neuroprotective effects in animals of different age with experimental models of nervous system pathology (Hardeland, 2012;Murioz-Jurado et al, 2022). The aim of study was:(1) to evaluate changes of the brain macrophages, astrocytes, T-cells, neural stem cells, neurons and CNS functioning in the neurotoxin cuprizone-treated mice of different age; and (2) to assess in such mice the effects of exogenous melatonin and possible courses of its action.…”