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Suchschritt : FT=glucosamine AND FT=osteoarthritis
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2/281 von 416 DIMDI: MEDLINE (ME60) © NLM

ND: | ME11229466
PMID: | 11229466
LR: | 20061115
CED: | 20010302
DCO: | 20010322
Autoren: | Gouze JN; Bordji K; Gulberti S; Terlain B; Netter P; Magdalou J; Fournel-Gigleux S; Ouzzine M
Titel: | Interleukin-1beta down-regulates the expression of glucuronosyltransferase I, a key enzyme priming glycosaminoglycan biosynthesis: influence of glucosamine on interleukin-1beta-mediated effects in rat chondrocytes.
Quelle: | Arthritis and rheumatism; VOL: 44 (2); p. 351-60 /200102/
PM: | Print
SU: | AIM IM
Sprache: | English
CY: | United States
JID: | 0370605
ISSN: | 0004-3591
CO: | ARHEAW
Institution: | CNRS-Université Henri Poincaré-Nancy I, Vandoeuvre-lés-Nancy, France.
DT: | Journal Article; Research Support, Non-U.S. Gov't
Schlagwörter
CT: | ANIMALS; CELLS, CULTURED; CHONDROCYTES/drug effects; CHONDROCYTES/metabolism; DINOPROSTONE/metabolism; DOWN-REGULATION/drug effects; GLUCOSAMINE/pharmacology; GLUCURONOSYLTRANSFERASE/*biosynthesis; GLUCURONOSYLTRANSFERASE/genetics; GLUCURONOSYLTRANSFERASE/*physiology; GLYCOSAMINOGLYCANS/*biosynthesis; INTERLEUKIN-1/*pharmacology; MALE; MATRIX METALLOPROTEINASE 3/genetics; NITRIC OXIDE/biosynthesis; OSTEOARTHRITIS/drug therapy; RNA, MESSENGER/metabolism; RATS; RATS, WISTAR
CTG: | TIER; ZELLEN, KULTIVIERTE; CHONDROZYTEN/Arzneimittelwirkungen; CHONDROZYTEN/Stoffwechsel; DINOPROSTON/Stoffwechsel; DOWN-REGULATION/Arzneimittelwirkungen; GLUCOSAMIN/Pharmakologie; GLUCURONOSYLTRANSFERASE/*Biosynthese; GLUCURONOSYLTRANSFERASE/Genetik; GLUCURONOSYLTRANSFERASE/*Physiologie; GLYCOSAMINO-GLYCANE/*Biosynthese; INTERLEUKIN-1/*Pharmakologie; MÄNNLICH; STROMELYSIN 1/Genetik; STICKSTOFFMONOXID/Biosynthese; OSTEOARTHROSE/Arzneimitteltherapie; RNA, MESSENGER-/Stoffwechsel; RATTUS; RATTEN, WISTAR-
TE: | Glycosaminoglycans; Interleukin-1; RNA, Messenger; glucosaminoglycans; Nitric Oxide/10102-43-9; Glucosamine/3416-24-8; Dinoprostone/363-24-6; galactosylgalactoylxylosylprotein 3-beta-glucuronosyltransferase/E.C. 2.4.1.135; Glucuronosyltransferase/E.C. 2.4.1.17; Matrix Metalloproteinase 3/E.C. 3.4.24.17
CR: | 10102-43-9; 3416-24-8; 363-24-6; E.C. 2.4.1.135; E.C. 2.4.1.17; E.C. 3.4.24.17
AB: | OBJECTIVE: To assess the variations of galactose-beta-1,3-glucuronosyltransferase I (GlcAT-I) expression related to the decrease in proteoglycan synthesis mediated by interleukin-1beta (IL-1beta) in rat chondrocytes, and to evaluate the influence of glucosamine on the effects elicited by this proinflammatory cytokine. METHODS: Rat articular chondrocytes in primary monolayer cultures or encapsulated into alginate beads were treated with recombinant IL-1beta in the absence or presence (1.0-4.5 gm/liter) of glucosamine. Variations of GlcAT-I and expression of stromelysin 1 (matrix metalloproteinase 3 [MMP-3]) messenger RNA (mRNA) were evaluated by quantitative multistandard reverse transcriptase-polymerase chain reaction. In vitro enzymatic activity of GlcAT-I was measured by thin-layer chromatography, with radiolabeled UDP-glucuronic acid and a digalactoside derivative as substrates. Proteoglycan synthesis was determined by ex vivo incorporation of Na2-35SO4. Nitric oxide synthase and cyclooxygenase activities were monitored by the evaluation of nitrite (NO2-) and prostaglandin E2 (PGE2) produced in the culture medium, respectively. RESULTS: IL-1beta treatment resulted in a marked inhibition of GlcAT-I mRNA expression and in vitro catalytic activity, together with a decrease in proteoglycan synthesis. In addition, glucosamine was able to prevent, in a dose-dependent manner, the inhibitory effects of IL-1beta. In the same way, the amino sugar reduced NO2- and PGE2 production induced by IL-1beta. Finally, the up-regulation of stromelysin 1 (MMP-3) mRNA expression by IL-1beta was fully prevented by glucosamine. CONCLUSION: The results of this study suggest that the deleterious effect of IL-1beta on the anabolism of proteoglycan could involve the repression of GlcAT-I, a key enzyme in the biosynthesis of glycosaminoglycan. Glucosamine was highly effective in preventing these IL-1beta-mediated suppressive effects. The amino sugar also prevented the production of inflammatory mediators induced by the cytokine. This action could account for a possible beneficial effect of glucosamine on osteoarthritic articular cartilage.

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