Papers of the Week

The mechanism of CFB in treating knee osteoarthritis is not yet clear and deserves further discussion. The C28/I2 cell was stimulated by TNF-α and the MIA-induced OA rat model were constructed, and then treated with a certain concentration of CFB. The effects of CFB on chondrocyte apoptosis, inflammatory response, and collagen matrix degradation were assessed. Furthermore, we analyzed the regulation of CFB on the DDIT3 and Hedgehog pathways through western blot analysis. The smoothened agonist inhibitor SAG and DDIT3 overexpression lentivirus were applied to investigate how CFB regulates DDIT3 and Hedgehog pathway to protect against osteoarthritis. Our experimental results proved the protective of CFB against TNF-α stimulated C28/I2 cells. CFB treatment downregulated the DDIT3 protein and inactivated the HH pathway in TNF-α stimulated C28/I2 cells, and this effect may be related to the DDIT3 or HH pathway. Furthermore, the inhibitory effect of CFB on the HH pathway is related to DDIT3. In vivo animal assays showed that CFB can inhibit the degradation of cartilage collagen matrix, inhibit chondrocyte apoptosis, improve chondrocyte damage, and alleviate pain in arthritis rats, and the effect of CFB on OA rats is related to the HH pathway mediated by DDIT3. In summary, CFB has significant therapeutic effects on osteoarthritis, protecting cartilage degradation and damage, and inhibiting inflammatory responses. DDIT3 may participate as an intermediate molecule in the protective effect of the drug on OA. The SHH/GLi1 pathway is regulated by CFB through DDIT3.