Abstract
BackgroundOsteoarthritis (OA) is a common joint disease that causes disabilities in elderly. However, few agents with high efficacy and low side effects have been developed to treat OA. In this study, we evaluated the effects of the alginate extract named CTX in OA cell and rabbit models.ResultsCTX was formulated by hydrolyzing sodium alginate polymers with alginate lyase and then mixing with pectin. HPLC was used to analyze the CTX content. Human chondrosarcoma SW1353 cells treated with interleukin-1β were used as OA model cells to investigate the effects of CTX on chondrocyte inflammation and anabolism. CTX at concentrations up to 1000 μg/ml exerted low cytotoxicity. It inhibited the gene expression of proinflammatory matrix metalloproteinases (MMPs) including MMP1, MMP3 and MMP13 in a dose-dependent manner and increased the mRNA level of aggrecan, the major proteoglycan in articular cartilage, at 1000 μg/ml. Thirteen-week-old New Zealand White rabbits underwent a surgical anterior cruciate ligament transection and were orally treated with normal saline, glucosamine or CTX for up to 7 weeks. Examinations of the rabbit femur and tibia samples demonstrated that the rabbits taking oral CTX at a dosage of 30 mg/kg/day suffered lesser degrees of articular stiffness and histological cartilage damage than the control rabbits.ConclusionsThe gene expression profiles in the cell and the examinations done on the rabbit cartilage suggest that the alginate extract CTX is a pharmaco-therapeutic agent applicable for OA therapy.
Highlights
Osteoarthritis (OA) is a common joint disease that causes disabilities in elderly
CTX inverted OA pathogenesis in vitro After the lyase hydrolyzation alginate polymers were converted into oligomers
Chondrosarcoma SW1353 cells were tested with different concentrations of the alginate extract CTX
Summary
Osteoarthritis (OA) is a common joint disease that causes disabilities in elderly. Few agents with high efficacy and low side effects have been developed to treat OA. The pathologic changes include proteoglycan degradation, type II collagen degradation, and eventually local or complete loss of the cartilage matrix [3]. Cytokines and their downstream targets are major players in the pathogenesis of OA [4, 5]. The development of OA therapeutics focuses primarily on disease-modifying OA drugs (DMOADs) and connective tissue structure-modifying agents (CTSMAs) [12,13,14,15]. Our team as well as others showed OA-relieving effects of injectable hyaluronan, a polysaccharide and major
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