Fig. 2.

The expression pattern of CST in OA and degenerative chondrocytes; CST treatment attenuates the severity of OA in the DMM model. (A-B) CST expression was diminished by TNF-α in chondrocytes, as determined through cell immunostaining and Real-time PCR. (C-D) The expression level of CST was diminished in OA cartilage. Cartilage samples were isolated from patients with or without OA, and Real-time PCR and western blotting were performed. (E-F) Levels of CST greatly decreased in DMM models, as observed through Real-time PCR and immunohistochemistry. (G) Intra-articular injection of CST remarkably protected the structure of the articular cartilage and maintained proteoglycan in the cartilage. The DMM model was established in WT mice with or without CST treatment, and the mice were sacrificed at the 4-week and 8-week time points. (H—K) CST suppressed OA development (measured by OARSI scoring), chondrocyte number, loss of proteoglycan (arbitrary units) and cartilage thickness (μm) (measured through histology). (L-P) Levels of OA-associated biomarkers, such as IL-1β, iNOS, COX-2, MMP-13 and ADAMTS-5, were diminished in the CST treatment group as assayed by Real-time PCR. (Q) Decreased IL-1β levels were found with CST treatment in DMM model mice through ELISA. (R) iNOS and COX-2 were found to be suppressed by CST treatment compared to a PBS vehicle control, as detected by western blot. (S) Treatment with CST downregulated the levels of ADAMTS-5 and MMP-13 in DMM model mice, according to immunohistochemical results of articular cartilage (*p < .05, **p < .01 vs control group). n = 7 for each group, Scale bar: 50 μm.