AIM: The aim was to study whether oral glucosamine hydrochloride (GlcN.HCl) or mucopolysaccharide protein (MucoP) has a structure-modifying effect on an anterior cruciate ligament transection (ACLT) rabbit model of osteoarthritis (OA). METHODS: OA was surgically induced in the right knees of rabbits by transection of the ACLT. The left knees served as a sham-operated control. The animals were divided into four groups (n = 6 each): negative control (phosphate buffered saline, orally), positive control (oral celecoxib 10 mg/kg body weight/day), GlcN.HCl (oral 100 mg/kg/day) and MucoP (oral 100 mg/kg/day). Experimental animals were sacrificed after 8 weeks of treatment and the distal femur was removed for macroscopic examination, histological assessment, and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assay of the OA rabbits. RESULTS: On gross morphology, severe lesions were observed in articular cartilage in the negative control group. In the GlcN.HCl and MucoP treatment groups, fibrillations and cartilaginous lesions were significantly (P < 0.05) decreased compared to the negative control group. In particular, degenerative changes in cartilage and chondrocyte cellularity were significantly reduced (P < 0.05) in the positive control (celecoxib) group, GlcN.HCl treatment group and MucoP treatment group compared with the negative control group. TUNEL assay showed that apoptotic chondrocytes were significantly suppressed in the celecoxib group. Similar significant (P < 0.05) results were seen in the GlcN.HCl group and MucoP group but apoptosis of chondrocytes were high in the negative control group. CONCLUSION: These data suggest that the protective effects of GlcN.HCl and MucoP may play a useful role in the clinical treatment of OA.
AIM: The aim was to study whether oral glucosamine hydrochloride (GlcN.HCl) or mucopolysaccharide protein (MucoP) has a structure-modifying effect on an anterior cruciate ligament transection (ACLT) rabbit model of osteoarthritis (OA). METHODS: OA was surgically induced in the right knees of rabbits by transection of the ACLT. The left knees served as a sham-operated control. The animals were divided into four groups (n = 6 each): negative control (phosphate buffered saline, orally), positive control (oral celecoxib 10 mg/kg body weight/day), GlcN.HCl (oral 100 mg/kg/day) and MucoP (oral 100 mg/kg/day). Experimental animals were sacrificed after 8 weeks of treatment and the distal femur was removed for macroscopic examination, histological assessment, and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assay of the OA rabbits. RESULTS: On gross morphology, severe lesions were observed in articular cartilage in the negative control group. In the GlcN.HCl and MucoP treatment groups, fibrillations and cartilaginous lesions were significantly (P < 0.05) decreased compared to the negative control group. In particular, degenerative changes in cartilage and chondrocyte cellularity were significantly reduced (P < 0.05) in the positive control (celecoxib) group, GlcN.HCl treatment group and MucoP treatment group compared with the negative control group. TUNEL assay showed that apoptotic chondrocytes were significantly suppressed in the celecoxib group. Similar significant (P < 0.05) results were seen in the GlcN.HCl group and MucoP group but apoptosis of chondrocytes were high in the negative control group. CONCLUSION: These data suggest that the protective effects of GlcN.HCl and MucoP may play a useful role in the clinical treatment of OA.