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Suchschritt : FT=glucosamine AND FT=osteoarthritis
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ND: | ME10608273
PMID: | 10608273
LR: | 20051117
CED: | 20000106
DCO: | 20000106
Autoren: | McCarty MF; Russell AL
Titel: | Niacinamide therapy for osteoarthritis--does it inhibit nitric oxide synthase induction by interleukin 1 in chondrocytes?
Quelle: | Medical hypotheses; VOL: 53 (4); p. 350-60 /199910/
PM: | Print
SU: | IM
Sprache: | English
CY: | ENGLAND
JID: | 7505668
ISSN: | 0306-9877
CO: | MEHYDY
Institution: | Nutrition 21/AMBI, San Diego, CA 92037, USA.
DT: | Journal Article
Schlagwörter
CT: | ANTIOXIDANTS/pharmacology; CARTILAGE, ARTICULAR/drug effects; CARTILAGE, ARTICULAR/enzymology; CARTILAGE, ARTICULAR/*metabolism; ENZYME INHIBITORS/*therapeutic use; FISH OILS/pharmacology; GLUCOSAMINE/pharmacology; HUMANS; HYALURONIC ACID/pharmacology; INTERLEUKIN-1/antagonists & inhibitors; INTERLEUKIN-1/*physiology; NIACINAMIDE/*therapeutic use; NITRIC OXIDE SYNTHASE/*antagonists & inhibitors; NITRIC OXIDE SYNTHASE/biosynthesis; OSTEOARTHRITIS/*drug therapy; S-ADENOSYLMETHIONINE/pharmacology; SIGNAL TRANSDUCTION
CTG: | ANTIOXYDANZIEN/Pharmakologie; KNORPEL, GELENK-/Arzneimittelwirkungen; KNORPEL, GELENK-/Enzymologie; KNORPEL, GELENK-/*Stoffwechsel; ENZYMINHIBITOREN/*therapeutische Anwendung; FISCHÖLE/Pharmakologie; GLUCOSAMIN/Pharmakologie; MENSCH; HYALURONSÄURE/Pharmakologie; INTERLEUKIN-1/Antagonisten & Inhibitoren; INTERLEUKIN-1/*Physiologie; NIACINAMID/*therapeutische Anwendung; STICKSTOFFMONOXID-SYNTHASE/*Antagonisten & Inhibitoren; STICKSTOFFMONOXID-SYNTHASE/Biosynthese; OSTEOARTHROSE/*Arzneimitteltherapie; S-ADENOSYLMETHIONIN/Pharmakologie; SIGNALÜBERTRAGUNG
TE: | Antioxidants; Enzyme Inhibitors; Fish Oils; Interleukin-1; S-Adenosylmethionine/29908-03-0; Glucosamine/3416-24-8; Hyaluronic Acid/9004-61-9; Niacinamide/98-92-0; Nitric Oxide Synthase/E.C. 1.14.13.39
CR: | 29908-03-0; 3416-24-8; 9004-61-9; 98-92-0; E.C. 1.14.13.39
AB: | Fifty years ago, Kaufman reported that high-dose niacinamide was beneficial in osteoarthritis (OA) and rheumatoid arthritis. A recent double-blind study confirms the efficacy of niacinamide in OA. It may be feasible to interpret this finding in the context of evidence that synovium-generated interleukin-1 (IL-1), by inducing nitric oxide (NO) synthase and thereby inhibiting chondrocyte synthesis of aggrecan and type II collagen, is crucial to the pathogenesis of OA. Niacinamide and other inhibitors of ADP-ribosylation have been shown to suppress cytokine-mediated induction of NO synthase in a number of types of cells; it is therefore reasonable to speculate that niacinamide will have a comparable effect in IL-1-exposed chondrocytes, blunting the anti-anabolic impact of IL-1. The chondroprotective antibiotic doxycycline may have a similar mechanism of action. Other nutrients reported to be useful in OA may likewise intervene in the activity or synthesis of IL-1. Supplemental glucosamine can be expected to stimulate synovial synthesis of hyaluronic acid; hyaluronic acid suppresses the anti-catabolic effect of IL-1 in chondrocyte cell cultures, and has documented therapeutic efficacy when injected intra-articularly. S-adenosylmethionine (SAM), another proven therapy for OA, upregulates the proteoglycan synthesis of chondrocytes, perhaps because it functions physiologically as a signal of sulfur availability. IL-1 is likely to decrease SAM levels in chondrocytes; supplemental SAM may compensate for this deficit. Adequate selenium nutrition may down-regulate cytokine signaling, and ample intakes of fish oil can be expected to decrease synovial IL-1 production; these nutrients should receive further evaluation in OA. These considerations suggest that non-toxic nutritional regimens, by intervening at multiple points in the signal transduction pathways that promote the synthesis and mediate the activity of IL-1, may provide a substantially superior alternative to NSAIDs (merely palliative and often dangerously toxic) in the treatment and perhaps prevention of OA.

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