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

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

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.

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