2001
DOI: 10.1016/s0014-5793(01)03255-0
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Glucosamine modulates IL‐1‐induced activation of rat chondrocytes at a receptor level, and by inhibiting the NF‐κB pathway

Abstract: We recently reported that glucosamine reversed the decrease in proteoglycan synthesis and in UDP-glucuronosyltransferase I mRNA expression induced by interleukin-1L L (IL-1L L) [Arthritis Rheum. 44 (2001) 351^360]. In the present work, we show that glucosamine does not exert the same effects when chondrocytes were stimulated with reactive oxygen species (ROS). In order to better understand its mechanism of action, we determined if glucosamine could prevent the binding of IL-1L L to its cellular receptors or co… Show more

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Cited by 146 publications
(112 citation statements)
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“…In addition, the potential immunoregulatory capacity of glucosamine has also been suggested. Indeed, glucosamine has been shown to suppress proinflammatory cytokine action in human chondrocytes (10), to inhibit NF-B activation and IL-1␤ bioactivity in rat chondrocytes (11), and to suppress unprimed T cell response by interfering with functions of APCs and by a direct inhibitory effect on CD3-induced T cell proliferation (12). Furthermore, the addition of glucosamine to immune cells in vitro prevented both their activation and their ability to initiate the MLR.…”
Section: E Xperimental Autoimmune Encephalomyelitis (Eae) 2 Is a Cd4mentioning
confidence: 99%
“…In addition, the potential immunoregulatory capacity of glucosamine has also been suggested. Indeed, glucosamine has been shown to suppress proinflammatory cytokine action in human chondrocytes (10), to inhibit NF-B activation and IL-1␤ bioactivity in rat chondrocytes (11), and to suppress unprimed T cell response by interfering with functions of APCs and by a direct inhibitory effect on CD3-induced T cell proliferation (12). Furthermore, the addition of glucosamine to immune cells in vitro prevented both their activation and their ability to initiate the MLR.…”
Section: E Xperimental Autoimmune Encephalomyelitis (Eae) 2 Is a Cd4mentioning
confidence: 99%
“…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%
“…Ainsi, la surexpression du TGFβ dans la membrane synoviale provoque l'apparition de fibroses pulmonaires massives nécessitant l'euthanasie de l'animal (données personnelles), tandis que le transfert de l'ADNc exprimant BMP2 a été suivi de formations osseuses ectopiques [29]. Une autre approche utilisant l'accumulation intracellulaire de glucosamine semble protéger les cellules contre les effets néfastes de l'IL-1 [30]. La glucosamine est utilisée de façon empirique dans le traitement de l'arthrose, et bien que ce ne soit pas une protéine, son accumulation est rendue possible par la surexpression de la glutamine fructose 6-phosphate-amido-transfé-rase (GFAT), enzyme impliquée dans sa biosynthèse.…”
Section: Pourquoi Avoir Développé De Nouvelles Thérapies Pour Les Malunclassified