Melatonin as an Anti-Inflammatory Agent Modulating Inflammasome Activation
TLDR
Melatonin is an important antioxidant and also a widespread anti-inflammatory molecule, modulating both pro- and anti- inflammatory cytokines in different pathophysiological conditions and its roles and its protective effects against the activation of the inflammasomes and, in particular, of the NLRP3 inflammaome are focused on.Abstract:
Inflammation may be defined as the innate response to harmful stimuli such as pathogens, injury, and metabolic stress; its ultimate function is to restore the physiological homeostatic state The exact aetiology leading to the development of inflammation is not known, but a combination of genetic, epigenetic, and environmental factors seems to play an important role in the pathogenesis of many inflammation-related clinical conditions Recent studies suggest that the pathogenesis of different inflammatory diseases also involves the inflammasomes, intracellular multiprotein complexes that mediate activation of inflammatory caspases thereby inducing the secretion of proinflammatory cytokines Melatonin, an endogenous indoleamine, is considered an important multitasking molecule with fundamental clinical applications It is involved in mood modulation, sexual behavior, vasomotor control, and immunomodulation and influences energy metabolism; moreover, it acts as an oncostatic and antiaging molecule Melatonin is an important antioxidant and also a widespread anti-inflammatory molecule, modulating both pro- and anti-inflammatory cytokines in different pathophysiological conditions This review, first, gives an overview concerning the growing importance of melatonin in the inflammatory-mediated pathological conditions and, then, focuses on its roles and its protective effects against the activation of the inflammasomes and, in particular, of the NLRP3 inflammasomeread more
Citations
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Melatonin and inflammation—Story of a double‐edged blade
TL;DR: A particular role in melatonin's actions seems to be associated with the upregulation of sirtuin‐1 (SIRT1), which shares various effects known from melatonin and additionally interferes with the signaling by the mechanistic target of rapamycin and Notch, and reduces the expression of the proinflammatory lncRNA‐CCL2.
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Melatonin Attenuates LPS-Induced Acute Depressive-Like Behaviors and Microglial NLRP3 Inflammasome Activation Through the SIRT1/Nrf2 Pathway
Burak Ibrahim Arioz,Bora Tastan,Emre Tarakcioglu,Kemal Ugur Tufekci,Melis Olcum,Nevin Ersoy,Alper Bagriyanik,Kursad Genc,Sermin Genc +8 more
TL;DR: Melatonin prevents LPS and Adenosine triphosphate (ATP) induced NLRP3 inflammasome activation in murine microglia in vitro, evidenced by inhibition ofNLRP3 expression, Apoptosis-associated speck-like protein containing a CARD (ASC) speck formation, caspase-1 cleavage and interleukin-1 β (IL-1β) maturation and secretion.
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Curcumin as an anti-inflammatory agent: Implications to radiotherapy and chemotherapy.
Bagher Farhood,Keywan Mortezaee,Nasser Hashemi Goradel,Neda Khanlarkhani,Ensieh Salehi,Maryam Shabani Nashtaei,Masoud Najafi,Amirhossein Sahebkar +7 more
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Melatonin as a master regulator of cell death and inflammation: molecular mechanisms and clinical implications for newborn care.
Anna Tarocco,Natascia Caroccia,Giampaolo Morciano,Mariusz R. Wieckowski,Gina Ancora,Giampaolo Garani,Paolo Pinton +6 more
TL;DR: Molecular pathways in which melatonin is considered a master regulator, with attention to cell death and inflammation mechanisms from basic, translational and clinical points of view in the context of newborn care are summarized.
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Impact of Circadian Disruption on Cardiovascular Function and Disease
Sarah Laxhmi Chellappa,Sarah Laxhmi Chellappa,Nina Vujovic,Nina Vujovic,Jonathan S. Williams,Frank A.J.L. Scheer,Frank A.J.L. Scheer +6 more
TL;DR: Understanding the mechanisms by which the circadian system regulates CV function, and which of these are affected by circadian disruption, may help to develop intervention strategies to mitigate CV risk.
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TL;DR: The manuscript and the Figures and Table are based on a manuscript originally written by Gordon C. Dickinson in 2012 and then edited by David I. Dickinson and revised by David A. Dickinson.