Further studies on the ability of glucosamine and chondroitin sulphate to regulate catabolic mediatorsin vitro

Effect of glucosamine and chondroitin sulfate on regulation of gene expression of proteolytic enzymes and their inhibitors in interleukin-1–challenged bovine articular cartilage explants

“…However, one major limitation to these studies is that concentrations of the nutraceuticals used have been quite high, ranging from 0.1 to 10 mg/mL. 14,21,[27][28][29][30][31][32][33][34][35][36] These concentrations are most probably not attainable in vivo in the blood or synovial fluid after administration of the nutraceuticals via the oral or IV routes. This is one reason given by rheumatologists for not advocating the use of these nutraceuticals.…”

The effects of three‐month oral supplementation with a nutraceutical and exercise on the locomotor pattern of aged horses

“…Multiple in vitro studies have reported that glucosamine (GS) and chondroitin sulfate (CS) possess anti‐inflammatory properties when tested on stressed equine chondrocytes or cartilage explants . However, until recently , serum and synovial fluid concentrations of these supplements after oral dosing were unknown, making it impossible to verify whether concentrations tested in vitro were actually attainable in vivo .…”

Oral joint supplements in the management of osteoarthritis

“…In this theory it is proposed that GU supplies excess basic building blocks for the synthesis of cartilage glycosaminoglycans (GAG) (Fenton et al 2000, Laverty et al 2005, Kelly 1998) and/or bypasses rate-limiting steps in GAG synthesis (Fenton et al 2000, Trumble 2005). In addition, these structure-modifying agents appear to counteract inflammation primarily through their inhibition of intermediate messengers, such as nuclear factor kappa B, nitric oxide and PGE 2 (Bassleer et al 1998a, Fenton et al 2000, Orth et al 2002, Largo et al 2003, Mello et al 2004, Nakamura et al 2004, Schlueter et al 2004, Neil et al 2005b, that mediate inflammatory responses, in addition to their previously described antianabolic and procatabolic effects. However, these structure-modifying agents have not been found to directly inhibit cyclooxygenase (COX) enzymes, in contrast to many antiarthritic medications (Seaver & Smith 2004).…”

“…Glucosamine and/or CS are thought to counteract cartilage degradation (Sandy et al 1998, Fenton et al 2000, Grande et al 2000, Lippiello et al 2000, Nerucci et al 2000, Orth et al 2002, Ilic et al 2003, Mello et al 2004, Dechant et al 2005, Neil et al 2005b by inhibiting degradative enzymes such as collagenase and aggrecanase (Wright 2001, Lippiello et al 2002, Orth et al 2002, Mello et al 2004, Chan et al 2005, and intermediary mediators, such as nitric oxide, prostaglandin E 2 and nuclear factor kappa B (Bassleer et al 1998a, Fenton et al 2000, Orth et al 2002, Byron et al 2003, Dodge et al 2005, Largo et al 2003, Mello et al 2004, Nakamura et al 2004, Schlueter et al 2004, Neil et al 2005b. Synthesis of ECM components is thought to be stimulated in the presence of GU and/or CS (Bassleer et al included a chondroitin sulfate product from bovine trachea and a complex of glycosaminoglycans and other nutrients from the sea mussel, Perna canaliculus.…”

“…There are no requirements of Good Manufacturing Practices (GMPs) for manufactures to guarantee high-quality and batch-to-batch consistency (Oke & McIlwraith 2008) and because there is no post-production monitoring of veterinary nutritional supplements, a myriad of poor quality supplements are available ). 1998a,b, Nerucci et al 2000, Noyszewski et al 2001, Lippiello 2003, Dechant et al 2005 by provision of substrate, which may be deficient through dilution or hypermetabolic states (Lippiello 2003); upregulation of gene expression (Grande et al 2000, Dodge & Jimenez 2003; stimulation of cellular receptors and cellular signaling mechanisms, such as CD44 involved in positive feedback (Bassleer et al 1998a, Esford et al 1998, Platt 2001; and inhibition of negative intermediary messengers, such as nuclear factor kappa B, nitric oxide and prostaglandin E 2 (PGE 2 ) (Bassleer et al 1998a, Fenton et al 2000, Orth et al 2002, Largo et al 2003, Mello et al 2004, Nakamura et al 2004, Schlueter et al 2004.…”