Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway

  • Front Immunol. 2023 Jul 20;14:1171150. doi: 10.3389/fimmu.2023.1171150.
Ruixuan Yu  1 ,  Yongjian Yuan  1 ,  Zhicheng Liu  1  2 ,  Long Liu  3 ,  Zhaoning Xu  4 ,  Yunpeng Zhao  1 ,  Chunwang Jia  1 ,  Pengfei Zhang  1 ,  Hang Li  1 ,  Yuhao Liu  1 ,  Yi Wang  5  6 ,  Weiwei Li  3 ,  Lin Nie  1 ,  Xuecheng Sun  7 ,  Yuhua Li  1 ,  Ben Liu  1 ,  Haichun Liu  1
Affiliations
  • 1. Department of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, China.
  • 2. The First Clinical Medical School, Shandong University, Jinan, Shandong, China.
  • 3. Department of Pathology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
  • 4. School of Nursing and Rehabilitation, Shandong University, Jinan, Shandong, China.
  • 5. Department of Plastic and Burns Surgery, The Second Hospital of Shandong University, Jinan, Shandong, China.
  • 6. Emergency Medicine Center, The Second Hospital of Shandong University, Jinan, Shandong, China.
  • 7. Department of Orthopedic Trauma, Weifang People's Hospital, Weifang, Shandong, China.
PMID: 37545495 DOI: 10.3389/fimmu.2023.1171150
Abstract

Wear debris-induced osteolysis, especially titanium (Ti) particles-induced osteolysis, is the most common cause of arthroplasty failure with no effective therapy. Previous studies have suggested that inflammation and impaired osteogenesis are associated with Ti particles -induced osteolysis. Selenium (Se) is an essential trace element in the human body, which forms selenomethionine (Se-Met) in nature, and selenoproteins has strong anti-inflammatory and antioxidant stress effects. In this study, the effects of Se-Met on Ti particles-induced osteolysis were observed and the potential mechanism was explored. We found that exogenous Se-Met relieved osteolysis induced by Ti particles in two animal models and MC3T3-E1 cells. We found that the addition of Se-Met effectively inhibited Ti particle-induced inflammation by regulating reactive oxygen species-dependent (ROS-dependent) NOD-like Receptor protein 3 (NLRP3) inflammasome activation. These therapeutic effects were abrogated in MC3T3-E1 cells that had received a β-catenin antagonist, suggesting that Se-Met alleviates inflammatory osteolysis via the β-catenin signaling pathway. Collectively, these findings indicated that Se-Met may serve as a potential therapeutic agent for treating Ti particle-induced osteolysis.

Keywords
NLRP3; inflammatory osteolysis; selenomethionine; titanium particle-induced osteolysis; β-catenin.
Products