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Ultra-small iron-based nanoparticles Mitigate rheumatoid arthritis inflammation via macrophage Repolarization and
Mingyue Yan1,2, Kehao Hou1,2, Jinpeng Zhao1,2
1Department of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Abstract:
The characteristic pathological manifestations of rheumatoid arthritis (RA) include inflammatory cell infiltration, abnormal synoviocyte proliferation, and progressive bone and cartilage destruction. An excessive buildup of reactive oxygen species (ROS) within the joints is a critical factor promoting RA pathological progression. In this study, we innovatively employed a hard template-restricted controlled sintering carbonization strategy to fabricate ultra-small Fe3O4@C nanoparticles with hierarchical structures. The ultra-small Fe3O4@C nanoparticles exhibit multiple natural enzyme-mimic catalytic activity, effectively diminishing intracellular ROS levels in macrophages, while also facilitating the polarization toward the M2 phenotype, and significantly suppresses the production of pro-inflammatory cytokines. Mechanistic investigations reveal that Fe3O4@C significantly suppresses ferroptosis in synoviocytes and chondrocytes through regulation of the SLC7A11/GPX4 signalling pathway, thereby alleviating synovial tissue erosion and promoting type II collagen synthesis. In the collagen-induced arthritis mouse model, Fe3O4@C exhibited remarkable anti-inflammatory and chondroprotective effects, providing an innovative nanozyme therapeutic approach for RA treatment.
Insights
This study introduces novel Fe3O4@C nanoparticles that reduce damaging reactive oxygen species (ROS) and inflammation. These nanozymes offer a promising new therapeutic strategy for rheumatoid arthritis (RA) by protecting cartilage and bone.
Area of Science:
- Biomedical Engineering
- Materials Science
- Immunology
Background:
- Rheumatoid arthritis (RA) involves joint inflammation, abnormal cell growth, and tissue degradation, driven by excessive reactive oxygen species (ROS).
- Current RA treatments face challenges in effectively managing inflammation and protecting joint structures.
Purpose of the Study:
- To develop and evaluate ultra-small Fe3O4@C nanoparticles as a novel nanozyme therapeutic for rheumatoid arthritis (RA).
- To investigate the anti-inflammatory and chondroprotective mechanisms of Fe3O4@C nanoparticles in RA.
Main Methods:
- Fabrication of ultra-small Fe3O4@C nanoparticles using a hard template-restricted controlled sintering carbonization strategy.
- Assessment of nanoparticle catalytic activity, ROS scavenging, macrophage polarization, and cytokine suppression.
- Evaluation of Fe3O4@C effects on synoviocyte and chondrocyte ferroptosis via the SLC7A11/GPX4 pathway.
- Testing in a collagen-induced arthritis (CIA) mouse model.
Main Results:
- Fe3O4@C nanoparticles demonstrated multi-enzyme mimic activity, effectively reducing intracellular ROS in macrophages.
- These nanoparticles promoted M2 macrophage polarization and suppressed pro-inflammatory cytokine production.
- Fe3O4@C inhibited ferroptosis in synoviocytes and chondrocytes, alleviating synovial erosion and enhancing type II collagen synthesis.
- In vivo studies showed significant anti-inflammatory and chondroprotective effects in the CIA mouse model.
Conclusions:
- The developed Fe3O4@C nanoparticles represent an innovative nanozyme therapeutic approach for RA.
- These nanoparticles effectively mitigate RA pathology by scavenging ROS, modulating immune responses, and protecting joint tissues.
- Fe3O4@C offers a promising strategy for RA treatment with significant anti-inflammatory and chondroprotective benefits.
