摘要

The aim of the present study was to investigate potential alterations in the articular cartilage in a rat model of monosodium iodoacetate (MIA)-induced osteoarthritis (OA) with or without treatment with moderate treadmill exercise. A total of 30 male Sprague-Dawley rats were randomly divided into three groups (n=10), including the control, OA and OA with treadmill exercise (OAE) groups. Rats were evaluated upon completing the treadmill exercise program (speed, 18 m/min; 30 min/day; 5 days/week for 4 weeks). Interleukin (IL)-1 and IL-4 levels in the serum and intra-articular lavage fluid (IALF) were measured by ELISA. Alterations in articular cartilage and synovium were also evaluated by histology, immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction. The results revealed that IL-1 in the serum and IALF decreased in the OAE group, whereas IL-4 increased, and histological evaluation indicated that the OAE group had a clear treatment response. However, the expression of type II collagen in the articular cartilage increased in the OAE group as compared with the OA group, whereas ADAMTS5 expression decreased. In contrast to light chain 3B (LC3B), the protein expression levels of BECLIN1 and sequestosome 1 (SQSTM1) were increased in the OA group. In addition, a significant increase was observed between OA and OAE groups in LC3B and SQSTM1 protein levels, whereas no change was observed in BECLIN1 levels between the OA and OAE groups in the superficial and deep zones. The results of western blotting demonstrated that LC3II was notably decreased in the OA group and partially increased in the OAE group. The mRNA expression levels of LC3B and SQSTM1 increased in the OA and OAE groups, with a significant difference observed between the two groups, while a concomitant decrease was detected in BECLIN1 levels. In conclusion, 30 min of treadmill exercise had an evident protective effect in the articular cartilage of rats with MIA-induced OA and may promote autophagy in the articular cartilage.