In the current study, the effect of glucosamine methyl ester on cartilage degeneration in osteoarthritis rat model was investigated.
Forty Sprague-Dawley rats were assigned into 5 groups of 8 animals each. Osteoarthritis was induced in 4 groups using medial parapatellar incision followed by anterior cruciate ligament transection and meniscectomy. Normal and model osteoarthritis groups were given normal saline. The three treatment groups received 2, 5 and 10 mg/kg doses of glucosamine methyl ester daily for one month.
Microscopic examination of the knee cartilage showed a significant reduction in degeneration score in the treatment groups. Enzyme-linked immunosorbent assay revealed inhibition of interleukin-1β expression and nitric oxide generation on treatment with glucosamine methyl ester. Expressions of matrix metalloproteinase-3 and -13 in the treatment groups were significantly lower compared to the model osteoarthritis group. Polymerase chain reaction revealed an increased expression of tissue inhibitor of metalloproteinases 1 on treatment of rats with glucosamine methyl ester. In the osteoarthritis rats treated with various doses of glucosamine methyl ester staining, the level of toluidine blue and Masson's trichrome increased. In addition, the level of type II collagen was also higher in the rats of treatment group. The level of proteoglycan, collagen and type II collagen in OA rats treated with 10 mg/kg doses was ~3.2- (p<0.01), 2.4- (p<0.02), and 3.6- (p<0.05) fold, respectively higher compared to the untreated animals.
Glucosamine methyl ester, therefore, prevents degeneration of cartilage in osteoarthritis rats. It exhibits its effect by promoting proteoglycan, collagen, type II collagen, tissue inhibitor of metalloproteinases 1, and decreasing matrix metalloproteinase. Therefore, glucosamine methyl ester exhibits therapeutic effect against osteoarthritis.