Osteoarthritis (OA) is characterized by progressive degeneration of cartilage, formation of cartilage at the cartilage edge, and remodeling of the subchondral bone. Pro-inflammatory cytokines [e.g., interleukin (IL)-1β] that induce inflammation and promote chondrocyte damage induce OA. Currently, the diagnosis of OA is commonly based on imaging examinations (e.g., X-ray) and evaluations of clinical symptoms; however, biomarkers that can effectively diagnose OA are currently not available. By studying the mechanism underlying OA cartilage injury and changes in the concentrations of the biomarkers procollagen type II carboxy-terminal propeptide (PIICP), collagen type-II C-telopeptide fragments (CTX-II), and type II collagen cleavage neoepitope (C2C) during pathogenesis, the present study established a theoretical basis for the evaluation and early diagnosis of OA. In an experiment, 10 ng/ml IL-1β was used to the treat chondrocyte-induced OA models in vitro for 0, 12, 24 and 48 h. Western blotting was used to detect the expression levels of matrix metalloproteinase (MMP)-3, MMP-13, and inducible nitric oxide synthase (iNOS) protein at each time-point. The concentrations of CTX-II, C2C, and PIICP in the cell culture supernatant were detected by ELISA kit. A biochemical kit was used to detect changes of nitric oxide (NO) in the cell culture supernatant. In addition, chondrocytes were treated with 10 ng/ml IL-1β for 0, 30, 60 and 90 min and the translocation and phosphorylation of the NF-κB pathway were investigated by western blotting. Following IL-1β stimulation, the NF-κB pathway was activated to increase the expression levels of MMPs and iNOS synthesis downstream of the pathway, resulting in an increased degradation of type II collagen (Col II). To sum up, pro-inflammatory IL-1β induced an OA chondrocyte model. During the development of OA, the expression of MMPs and NO increased and Col II was degraded.
Keywords: chondrocyte; matrix metalloproteinases; osteoarthritis; rat; type II collagen.
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