Feprazone Mitigates IL-1β-Induced Cellular Senescence in Chondrocytes

This study aims to investigate whether Feprazone has a protective effect against interleukin-1 β -induced cellular senescence in human chondrocytes

Zhusong Huang; Jinfu Lan; Xi Gao


Scholarcy highlights

  • Osteoarthritis is a joint disease commonly observed in the elderly population and sportsmen
  • The process of cell senescence is accelerated by these proinflammatory factors through inhibiting the cell cycle and the inflammatory cascade signaling in the inflammatory cells
  • An in vitro cell senescence model in the human chondrocytes was successfully established by stimulation with interleukin-1 β and verified by the upregulation of SAβ-Gal, activated telomerase activity, G0/G1 phase arrest, elevated expressions of senescence-related proteins, and the activated NF-κB signaling pathway
  • By the introduction of Feprazone, we found that the cell senescence in the chondrocytes was significantly alleviated
  • We further investigated the expressions of matrix metalloproteinase-13 and ADAMTS-5, which are the inducers of the degradation of the extracellular matrix and reported to be involved in the development and progression of OA
  • We found that the elevated expressions of MMP-13 and ADAMTS-5 in the chondrocytes induced by IL-1β were significantly reversed by Feprazone, indicating a promising inhibitory effect of Feprazone against the degradation of ECM
  • Our data indicate that Feprazone mitigates interleukin-1 β-induced cellular senescence in chondrocytes through upregulating Nrf

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