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CAT/SOD-Enriched Achyranthes bidentata nanovesicles mitigate TMJOA via ROS scavenging and JNK/FOXO1 pathway
Rui Li1, Zhiqing Huang1, Lingyunbo Kong1
1Department of Temporomandibular Joint, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction & Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Achyranthes bidentata nanovesicles (ABNVs) show promise for treating temporomandibular joint osteoarthritis (TMJOA). These nanovesicles reduce inflammation and cartilage damage by clearing reactive oxygen species (ROS) and modulating macrophage activity.
Area of Science:
- Biomaterials Science
- Nanomedicine
- Osteoarthritis Research
Background:
- Temporomandibular joint osteoarthritis (TMJOA) is an inflammatory condition with limited therapeutic interventions.
- Oxidative stress significantly contributes to TMJOA pathogenesis, suggesting antioxidant strategies as potential treatments.
Purpose of the Study:
- To investigate the therapeutic potential of exosome-like nanovesicles derived from Achyranthes bidentata (ABNVs) for TMJOA.
- To elucidate the underlying mechanisms of ABNV action in mitigating TMJOA progression.
Main Methods:
- Isolation and characterization of ABNVs, assessing size, surface charge, and antioxidant enzyme content (catalase, superoxide dismutase).
- Evaluation of ABNV efficacy in a rat TMJOA model, analyzing cartilage and bone integrity, synovial inflammation, and macrophage polarization.
- In vitro studies on chondrocytes and macrophages to assess ABNV effects on inflammation, chondrogenesis, and reactive oxygen species (ROS) scavenging via JNK/FOXO1 pathway modulation.
Main Results:
- ABNVs demonstrated significant reduction in cartilage degradation, bone damage, and synovial inflammation in the TMJOA rat model.
- ABNVs suppressed M1 macrophage polarization and chondrocyte inflammation while not impairing chondrogenic differentiation.
- Mechanistically, ABNVs scavenged ROS via catalase/superoxide dismutase, modulated the JNK/FOXO1 pathway, and inhibited M1 macrophage activation.
Conclusions:
- ABNVs possess therapeutic potential for TMJOA by targeting oxidative stress and inflammation.
- ABNVs offer a novel strategy for TMJOA treatment through ROS scavenging and modulation of macrophage-mediated inflammation.
- The findings highlight ABNVs as a promising biomaterial for managing TMJOA by addressing key pathological pathways.

