Salidroside ameliorates lipopolysaccharide-induced ferroptosis in chondrocytes via regulation of the sirt1/foxo1 axis

Salidroside (SAL) is a bioactive constituent extracted from Rhodiola rosea plant and exerts antioxidant and anti-inflammatory properties. However, understanding of SAL for the treatment of arthritis is limited. The aim of the present study was to investigate whether SAL treats lipopolysaccharide (LPS)-induced chondrocyte injury by modulating the sirt1 silent information regulator 1)/FoxO1 (forkhead transcription factors O1) signaling pathway. Network pharmacology was used to screen the potential pathway of SAL for the treatment of osteoarthritis via the ferroptosis pathway. Subsequently, a chondrocyte inflammation model was established in vitro using LPS and SAL was used as a drug treatment. Effects of SAL treatment of chondrocytes was evaluated by western blot analysis, fluorescence, cell viability and oxidative assay. Analysis revealed that SAL significantly attenuated LPS-induced apoptosis and accumulation of oxides in chondrocytes, thereby protecting the integrity of cartilage extracellular matrix. In addition, SAL promoted the activation of the sirt1/foxo1 signaling cascade, which alleviated LPS-induced ferroptosis in chondrocytes. The present study demonstrated that SAL attenuated LPS-induced chondrocyte ferroptosis by regulating the sirt1/foxo1 pathway. This may provide a potential therapeutic avenue for cartilage damage in osteoarthritis.