Alleviates Inflammatory Response, Apoptosis, and ECM Degradation in Osteoarthritic Chondrocytes by Stabilizing .

BACKGROUND

It has been reported that Sirtuin 2 () prevents phosphoenolpyruvate carboxykinase 1 () degradation, which can be involved in aging-induced osteoarthritis (OA), but the molecular mechanism of / in chondrocytes has not been clarified. Therefore, this study aims to explore the mechanism of / in chondrocyte inflammation.

METHOD

To establish the OA model , chondrocytes cultured with interleukin-1β (IL-1β, 10 ng/mL) and manipulation of and expression in the constructed cells to elucidate the interaction between the two genes. 1,9-Dimethyl-Methylene Blue (DMMB) was used to detect cellular glycosaminoglycan (GAG) content. Inflammatory factor levels were assessed using Enzyme-linked Immunosorbent Assay (ELISA). Apoptosis was detected by osmotic dye. The expression of B-cell lymphoma-2 (Bcl-2), Bcl-2 Associated X (Bax), Wnt Family Member 1 (Wnt1), catenin Beta 1 (β-catenin), Aggrecan, Collagen II, matrix metallopeptidase 13 (MMP-13) proteins in cells were analyzed using Western blot.

RESULTS

gained lower expressions in OA cell models. Overexpression of or S in the IL-1β chondrocyte model of inflammation promoted GAG content, inhibited apoptosis and Wnt/β-catenin protein expression, and lowered the levels of inflammatory factors. silencing was proved to have the opposite effect. overexpression rescued the increased inflammation, MMP-13 expression, and apoptosis and the decreased Aggrecan and Collagen II expression caused by silencing. silencing also reversed the positive effects of overexpression on chondrocytes.

CONCLUSION

inhibits articular chondrocyte extracellular matrix (ECM) degradation, inflammatory factor expression, and apoptosis via .