Glucosamine inhibits IL-1β-induced NFκB activation in human osteoarthritic chondrocytes

Largo, Raquel; Alvarez-Soria, M A; Díez-Ortego, I; Calvo, Emílio; Sánchez‐Pernaute, Olga; Egido, Jesús; Herrero‐Beaumont, Gabriel

doi:10.1016/s1063-4584(03)00028-1

Cited by 363 publications

(313 citation statements)

References 33 publications

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“…Isolation of PBMCs was done by Lymphoprep separation (28), and cell pellets were lysed in hypotonic buffer for nuclear protein isolation (35) or in TRIzol reagent (Life Technologies, Gaithersburg, MD) for RNA extraction. Protein extracts pooled from mononuclear cells were prepared as described previously (28), and the concentration was quantified by the bicinchoninic acid method (Pierce, Rockford, IL).…”

Section: Serum Chemistrymentioning

confidence: 99%

“…Protein extracts pooled from mononuclear cells were prepared as described previously (28), and the concentration was quantified by the bicinchoninic acid method (Pierce, Rockford, IL). A consensus oligonucleotide for NF-B (Promega, Madison, WI) was 32 P end-labeled using 10 units of T4 polynucleotide kinase (Promega), and nuclear extracts were equilibrated in binding buffer (35) before adding the labeled probe. The specificity of the assay was tested by preincubating the samples with a 100-fold excess of unlabeled probe (competitive control).…”

Section: Serum Chemistrymentioning

confidence: 99%

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Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Largo

Sánchez‐Pernaute

Marcos

et al. 2008

Arthritis & Rheumatism

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Objective. To determine whether systemic inflammation induced by chronic antigen-induced arthritis (AIA) accelerates vascular lesions in rabbits with atherosclerosis.Methods. Two models of atherosclerosis and chronic AIA were combined. Atherosclerosis was induced by coupling a hyperlipemic diet with an endothelial lesion at the femoral arteries, while chronic AIA was induced by ovalbumin injection. Markers in sera and peripheral blood mononuclear cells (PBMCs) as well as vessels and synovial membranes from the rabbits with the double phenotype (both chronic AIA and atherosclerosis) were compared with those from rabbits with each disease alone.Results. Serum levels of interleukin-6, C-reactive protein, and prostaglandin E 2 increased in rabbits with both chronic AIA and atherosclerosis as compared with healthy animals or animals with either chronic AIA alone or atherosclerosis alone. NF-B binding and CCL2 and cyclooxygenase 2 (COX-2) expression were higher in PBMCs from rabbits with both chronic AIA and atherosclerosis than in PBMCs from healthy rabbits. The intima-media thickness ratio of femoral arteries was equally increased in rabbits with atherosclerosis alone and in rabbits with both chronic AIA and atherosclerosis, but the latter group showed a higher level of macrophage infiltration. Femoral CCL2 and COX-2 expression was increased in rabbits with both chronic AIA and atherosclerosis as compared with rabbits with atherosclerosis alone. In the aortas, vascular lesions were found in 27% of rabbits with atherosclerosis alone and in 60% of rabbits with both chronic AIA and atherosclerosis. Rabbits with both chronic AIA and atherosclerosis exhibited more severe synovitis and higher synovial expression of CCL2 than did rabbits with chronic AIA alone.Conclusion. The onset of chronic AIA in animals with atherosclerosis resulted in the local and systemic up-regulation of mediators of tissue inflammation and plaque instability associated with a higher incidence of aortic lesions. This model could represent a novel approach to the study of inflammation-associated atherosclerosis.

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Section: Serum Chemistrymentioning

confidence: 99%

Section: Serum Chemistrymentioning

confidence: 99%

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Largo

Sánchez‐Pernaute

Marcos

et al. 2008

Arthritis & Rheumatism

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“…At the cellular level, GlcN inhibits interleukin-1␤ (IL-1␤)-induced nuclear factor-B (NF-B) activation in chondrocytes (10,11). As well, GlcN inhibits lipopolysaccharide (LPS)-induced NO production in RAW 264.7 macrophages and microglia (10 -14).…”

mentioning

confidence: 99%

Lipopolysaccharide (LPS)-stimulated iNOS Induction Is Increased by Glucosamine under Normal Glucose Conditions but Is Inhibited by Glucosamine under High Glucose Conditions in Macrophage Cells

Hwang

Kwon

Kim

et al. 2017

Journal of Biological Chemistry

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Edited by Dennis R. VoelkerWe investigated the regulatory effect of glucosamine (GlcN) for the production of nitric oxide (NO) and expression of inducible NO synthase (iNOS) under various glucose conditions in macrophage cells. At normal glucose concentrations, GlcN dose dependently increased LPS-stimulated production of NO/iNOS. However, GlcN suppressed NO/iNOS production under high glucose culture conditions. Moreover, GlcN suppressed LPS-induced up-regulation of COX-2, IL-6, and TNF-␣ mRNAs under 25 mM glucose conditions yet did not inhibit upregulation under 5 mM glucose conditions. Glucose itself dose dependently increased LPS-induced iNOS expression. LPS-induced MAPK and IB-␣ phosphorylation did not significantly differ at normal and high glucose conditions. The activity of LPS-induced nuclear factor-B (NF-B) and DNA binding of c-Rel to the iNOS promoter were inhibited under high glucose conditions in comparison with no significant changes under normal glucose conditions. In addition, we found that the LPS-induced increase in O-GlcNAcylation as well as DNA binding of c-Rel to the iNOS promoter were further increased by GlcN under normal glucose conditions. However, both O-GlcNAcylation and DNA binding of c-Rel decreased under high glucose conditions. The NF-B inhibitor, pyrrolidine dithiocarbamate, inhibited LPS-induced iNOS expression under high glucose conditions but it did not influence iNOS induction under normal glucose conditions. In addition, pyrrolidine dithiocarbamate inhibited NF-B DNA binding and c-Rel O-GlcNAcylation only under high glucose conditions. By blocking transcription with actinomycin D, we found that stability of LPS-induced iNOS mRNA was increased by GlcN under normal glucose conditions. These results suggest that GlcN regulates inflammation by sensing energy states of normal and fuel excess.

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“…Various cytokines such as nitric oxide, PG, interleukin-1β, tumor necrosis factor-α, interleukin-6 and interleukin-8 are expressed in higher proportions in the chondrocytes of OA patients [6,9]. Chondrocytes play an important role in the onset of pain during inflammation by activating the neurons [7,16]. Studies have demonstrated that the expressions of interleukin-4, tumor necrosis factor-α, interleukin-6, and interleukin-13 are promoted by P2X7R activation [17].…”

Section: Discussionmentioning

confidence: 99%

“…The development and progression of OA are induced by the expression of cytokines through alteration in the equilibrium between formation and degradation of chondrocytes [6]. Up-regulation of interleukin-13 leads to the breakdown of cartilage matrix and affects chondrocyte function [6,7]. The chondrocytes and synovial membrane of OA patients express higher level of interleukin-1β, interleukin-6, tumor necrosis factor-α and prostaglandin E2 [8].…”

Section: Introductionmentioning

confidence: 99%

Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

He¹,

Li²,

Li³

et al. 2018

Trop. J. Pharm Res

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Glucosamine inhibits IL-1β-induced NFκB activation in human osteoarthritic chondrocytes

Abstract: GS inhibits the synthesis of proinflammatory mediators in HOC stimulated with IL-1beta through a NFkappaB-dependent mechanism. Our study further supports the role of GS as a symptom- and structure-modifying drug in the treatment of OA.

Cited by 363 publications

References 33 publications

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Lipopolysaccharide (LPS)-stimulated iNOS Induction Is Increased by Glucosamine under Normal Glucose Conditions but Is Inhibited by Glucosamine under High Glucose Conditions in Macrophage Cells

Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

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