Adiponectin Induces Oncostatin M Expression in Osteoblasts through the PI3K/Akt Signaling Pathway.

摘要: Rheumatoid arthritis (RA), a common autoimmune disorder, is associated with chronic inflammatory response and unbalanced bone metabolism within the articular microenvironment. Adiponectin, an adipokine secreted by adipocytes, involved in multiple functions, including lipid pro-inflammatory activity. However, mechanism of adiponectin performance arthritic inflammation remains unclear. In this study, we observed effect on expression oncostatin M (OSM), cytokine, human osteoblastic cells. Pretreatment cells inhibitors phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor (NF)-κB reduced adiponectin-induced OSM osteoblasts. Stimulation increased phosphorylation PI3K, p65. Adiponectin treatment osteoblasts OSM-luciferase activity p65 binding to NF-κB promoter. Our results indicate that via signaling pathways cells, suggesting novel target for treatment.