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Neuroinflammation produced by heavy alcohol intake is due to loops of interactions between Toll-like 4 and TNF receptors, peroxisome proliferator-activated receptors and the central melanocortin system: A novel hypothesis and new therapeutic avenues

dc.contributor.authorFlores-Bastías O.
dc.contributor.authorKarahanian E.
dc.date.accessioned2020-09-02T22:17:53Z
dc.date.available2020-09-02T22:17:53Z
dc.date.issued2018
dc.identifier10.1016/j.neuropharm.2017.11.003
dc.identifier.citation128, , 401-407
dc.identifier.issn00283908
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4487
dc.descriptionExcessive alcohol intake induces an inflammatory response in the brain, via TNFα, TLR4 and NF-κB signaling pathways. It has been proposed that neuroinflammation would play a very important role in the development of alcohol addiction. In addition to stimulating the synthesis of inflammatory mediators such as IL-6, IL-1β and TNFα, NF-κB is capable of reducing the anti-inflammatory activity of PPARα and PPARγ. Reciprocally, PPARα, PPARγ and melanocortin 4 receptor (MC4R) can decrease the proinflammatory activity of NF-κB, establishing an interplay of inactivations between such nuclear factors and receptors. In this review, we hypothesize that one of the mechanisms by which alcohol produces neuroinflammation is through NF-κB-mediated decrease in PPARα and PPARγ anti-inflammatory activities; in addition, ethanol negatively affects MC4R activity, decreasing the ability of this receptor to activate PPARγ. PPARα, PPARγ and MC4R can be pharmacologically activated by synthetic ligands (fibrates, thiazolidinediones and synthetic peptides, respectively); in this context, we propose that the administration of such ligands would decrease neuroinflammation produced by alcohol intake. The advantage of this approach is that fibrates and thiazolidinediones are FDA-approved drugs that have been used for years in other clinical conditions, and now may offer a new perspective for the treatment of alcoholism. © 2017 Elsevier Ltd
dc.language.isoen
dc.publisherElsevier Ltd
dc.subjectAnti-inflammation
dc.subjectEthanol intake
dc.subjectMC4R
dc.subjectMelanocortin system
dc.subjectNeuroinflammation
dc.subjectPPAR
dc.subjectTLR4
dc.subject2,4 thiazolidinedione derivative
dc.subjectalcohol
dc.subjectfibric acid derivative
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectmelanocortin 4 receptor
dc.subjectperoxisome proliferator activated receptor alpha
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectsynthetic peptide
dc.subjecttoll like receptor 4
dc.subjecttumor necrosis factor receptor
dc.subjectalcohol
dc.subjectantiinflammatory agent
dc.subjectligand
dc.subjectmelanocortin
dc.subjectperoxisome proliferator activated receptor
dc.subjecttoll like receptor
dc.subjecttumor necrosis factor receptor
dc.subjectalcohol abuse
dc.subjectalcohol consumption
dc.subjectalcoholism
dc.subjectantiinflammatory activity
dc.subjecthuman
dc.subjectligand binding
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein protein interaction
dc.subjectShort Survey
dc.subjectanimal
dc.subjectchemically induced
dc.subjectdrinking behavior
dc.subjectinflammation
dc.subjectmetabolism
dc.subjectpathophysiology
dc.subjectAlcohol Drinking
dc.subjectAnimals
dc.subjectAnti-Inflammatory Agents
dc.subjectEthanol
dc.subjectHumans
dc.subjectInflammation
dc.subjectLigands
dc.subjectMelanocortins
dc.subjectPeroxisome Proliferator-Activated Receptors
dc.subjectReceptors, Tumor Necrosis Factor
dc.subjectToll-Like Receptors
dc.titleNeuroinflammation produced by heavy alcohol intake is due to loops of interactions between Toll-like 4 and TNF receptors, peroxisome proliferator-activated receptors and the central melanocortin system: A novel hypothesis and new therapeutic avenues
dc.typeShort Survey


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