The present study assessed the therapeutic efficacy of glucosamine hydrochloride against collagen-induced arthritis in female Dark Agouti rats (DA). Arthritis was induced by intradermaly injecting a collagen and complete Freund’s adjuvant suspension at multiple sites in the rat at a dose of 4？mg/kg of body weight and thereafter followed by two more boosters of the same dose, after the 1st week and 2nd week of primary immunization. After 21 days from the day of primary immunization, the arthritic group rats were given oral supplementation of glucosamine hydrochloride at a dose of 300？mg/kg of body weight until day 45. The arthritic group treated with glucosamine hydrochloride from day 21 to day 45 showed significant reduction in arthritic histopathological changes of the joints, reduction in paw thickness and also a significant decrease in C-reactive protein and TNF-alpha in the serum. Treatment with 300？mg/kg of glucosamine hydrochloride was able to reverse the arthritic changes, hence suggesting that glucosamine has a therapeutic effect against collagen-induced arthritis. 1. Introduction Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease. It is a destructive polyarthropathy that leads to disability and immobility [1]. The main characteristic feature of RA is swelling of the joints, and it is also sometimes manifested in other organ systems in severe disease states. Some of the common physical symptoms of RA are swelling of joint areas, painful and stiff joints, fatigue, malaise, weight, loss and sometimes even depression [2]. The exact aetiopathogenesis of RA is not known. Risk factors such as genetic predisposition and environmental factors like cigarette smoking [3], microbial infections [4], and blood transfusions [5] will lead to the activation of CD 4+ T helper cells, which will lead to the stimulation of various cells in the joints that produce cytokines and inflammatory mediators that play an important role in the development of RA. Inflammatory mediators like matrix metalloproteinases (MMP) and cell adhesion molecules (CAMs), together with cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1), lead to joint destruction in RA patients [2, 6]. At present, there are few treatment options available for RA. Nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase-2-selective NSAIDs [7], glucocorticoids, biological response modifying agents, and disease modifying antirheumatic drugs (DMARDs) are prescribed by physicians currently as single therapy or combined multiple drug therapy [8]. It has beenshown
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