Salidroside ameliorates lipopolysaccharide‑induced ferroptosis in chondrocytes via regulation of the sirt1/foxo1 axis
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- Published online on: March 26, 2025 https://doi.org/10.3892/mmr.2025.13502
- Article Number: 138
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Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
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.
