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Table 2 Principal characteristics of the in vitro studies testing glucosamine

From: Is there any scientific evidence for the use of glucosamine in the management of human osteoarthritis?

Model Concentration Results Reference
Glucosamine sulfate    
   Human OA chondrocytes 5-500 μM Inhibition of PLA2 and collagenase in a lesser extent through PKC inhibition [12]
   Human OA chondrocytes stimulated with IL-1β 10-1,000 mg/L Inhibition of NF-κB activation Inhibition of COX-2 expression and synthesis and PGE2 release [17]
   Human chondrocytes stimulated with IL-1β 10 mM Influence of the proteomic profile [20]
   Human OA cartilage explants 5 mM Inhibition of catabolic and anabolic gene expression Superiority over glucosamine hydrochloride in the same conditions [25]
   Human OA osteoblasts 200 μg/ml Inhibition of pro-resorptive agents [24]
Glucosamine hydrochloride    
   Transfected cell lines 10 mM Inhibition of ADAMTS-5 expression and activity [13]
   Human OA synovium explants 0.5-5 mM Induction of HA production No effect of N-acetylglucosamine [22]
   Rat chondrosarcoma cell line and 2-16 mM Inhibition of aggrecanase-dependent cleavage [11]
   bovine cartilage explants    
   Rat chondrocytes stimulated with IL-1β g/L 1-4.5 Reversion of IL-1β deleterious effect on PG anabolism [14]
   Rat chondrocytes stimulated with IL-1β 4.5 g/L Inhibition of NF-κB [16]
   Rat chondrocytes stimulated with IL-1β 20 mM Inhibition of inflammatory cytokines, chemokines and growth factors Inhibition of MMPs and aggrecanase-1 [15]
   Human synovial cells and chondrocytes 0.1-1.0 mM Stimulation of HA and GAG production Stimulation of HA synthase activity No effect of N-acetylglucosamine [21]
   Human chondrocytes stimulated with IL-1β 10 mM Inhibition of iNOS, COX-2 and IL-6 expression [18]
   Human chondrocytes 5-20 mM Increased synthesis of GAG and HA due to acceleration of facilitated glucose uptake Superiority over native glucosamine [26]
   Human chondrocytes (normal and OA) stimulated with IL-1β 2 mM Prevention of the cytokine-induced demethylation of CpG site in the IL-1β promoter resulting in decreased expression of IL-1β [19]
  1. ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs 5; COX-2, cyclooxygenase-2; GAG, glycosaminoglycan; HA, hyaluronic acid; iNOS, inducible nitric oxide synthase; MMP, matrix metalloproteinase; OA, osteoarthritis; PG, proteoglycan; PKC, protein kinase C; PGE2, prostaglandin E2; PLA2, phospholipase A2.