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Title: Lipopolysaccharide Binding Protein and Oxidative Stress in a Multiple Sclerosis Model.
Authors: Escribano, Begoña M
Medina-Fernández, Francisco J
Aguilar-Luque, Macarena
Agüera, Eduardo
Feijoo, Montserrat
Garcia-Maceira, Fe I
Lillo, Rafael
Vieyra-Reyes, Patricia
Giraldo, Ana I
Luque, Evelio
Drucker-Colín, René
Túnez, Isaac
Keywords: Dimethyl fumarate;Experimental autoimmune encephalomyelitis;Lipopolysaccharide binding protein;Natalizumab;Oxidative stress;Relapsing-remitting multiple sclerosis
metadata.dc.subject.mesh: Acetylcysteine
Acute-Phase Proteins
Carrier Proteins
Cell Count
Dimethyl Fumarate
Encephalomyelitis, Autoimmune, Experimental
Lipid Peroxidation
Membrane Glycoproteins
Middle Aged
Multiple Sclerosis
Oxidative Stress
Spinal Cord
Issue Date: 2017
Abstract: Recent findings in experimental autoimmune encephalomyelitis (EAE) suggest that altering certain bacterial populations present in the gut may lead to a proinflammatory condition, that could result in the development of multiple sclerosis (MS). Also, Reactive Oxygen Species seem to be involved in the course of MS. In this study, it has been aimed to relate all these variables starting from an analysis of the lipopolysaccharide (LPS) and LPS-binding protein (LBP) with the determination of parameters related to oxidative stress in the blood, brain and spinal cord. For this purpose, samples obtained from EAE rats and relapsing-remitting (RRMS) MS patients were used. In addition, EAE rats were treated with Natalizumab, N-acetyl-cysteine and dimethyl fumarate. Natalizumab was also employed in RRMS. The results of this study revealed an improvement in the clinical symptoms of the EAE and MS with the treatments, as well as a reduction in the oxidative stress parameters and in LBP. Correlations between the clinical variables of the disease, i.e. oxidative damage and LBP, were established. Although the conclusions of this research are indeed relevant, further investigation would be necessary to establish the intrinsic mechanisms of the MS-oxidative stress-microbiota relationship.
metadata.dc.identifier.doi: 10.1007/s13311-016-0480-0
Appears in Collections:Producción 2020

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