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Peroxiredoxin 4 inhibits IL-1β-induced chondrocyte apoptosis via PI3K/AKT signaling

Zhitao Rao1, Shuqing Wang1, Jiaqi Wang1

  • 1Department of Orthopaedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 20065, China.

Abstract

Insights

Peroxiredoxin 4 (PRDX4) protects against osteoarthritis by reducing reactive oxygen species (ROS) and preventing chondrocyte apoptosis. PRDX4

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Medicine

Background:

  • Osteoarthritis (OA) pathogenesis involves chondrocyte apoptosis driven by reactive oxygen species (ROS).
  • Peroxiredoxin 4 (PRDX4) is crucial for mitigating intracellular ROS levels.
  • Understanding PRDX4's role in interleukin 1β (IL-1β)-induced chondrocyte apoptosis is key for OA research.

Purpose of the Study:

  • To investigate the protective effects of PRDX4 against IL-1β-induced apoptosis in chondrocytes.
  • To elucidate the molecular mechanisms underlying PRDX4's function in chondrocyte survival.

Main Methods:

  • Primary rat chondrocytes were cultured and manipulated to overexpress PRDX4.
  • Cells were treated with IL-1β, and apoptosis, ROS production, nitric oxide (NO) levels, and protein expression were analyzed.
  • Western blotting, flow cytometry, and colorimetric assays were employed.

Main Results:

  • PRDX4 overexpression significantly reduced IL-1β-induced chondrocyte apoptosis.
  • PRDX4 reversed IL-1β-mediated increases in ROS and NO production.
  • PRDX4 modulated the expression of apoptosis-related proteins (Bcl-2, Bax) and activated the AKT signaling pathway.

Conclusions:

  • PRDX4 exerts protective effects against IL-1β-induced chondrocyte apoptosis, partly via the phosphatidylinositol 3-kinase/AKT pathway.
  • PRDX4 demonstrates potential as a therapeutic target for mitigating cartilage degeneration in osteoarthritis.

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