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Updated: Dec 17, 2025
Ameliorating Osteoarthritis in Mice Using Silver Nanoparticles
Published on: June 2, 2023
Nomilin targets the Keap1-Nrf2 signalling and ameliorates the development of osteoarthritis
Xing-He Xue1,2,3, Ji-Xin Xue1,2,3, Wei Hu1,2,3
1Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Abstract:
Osteoarthritis (OA) is a long-term and inflammatory disorder featured by cartilage erosion. Here, we describe nomilin (NOM), a triterpenoid with inflammation modulatory properties in variety of disorders. In this study, we demonstrated the latent mechanism of NOM in alleviating the progress of OA both in vitro and in vivo studies. The results showed that NOM pre-treatment suppressed the IL-1β-induced over-regulation of pro-inflammation factors, such as NO, IL-6, PGE2 , iNOS, TNF-α and COX-2. Moreover, NOM also down-regulates the degradation of ECM induced by IL-1β. Mechanistically, the NOM suppressed NF-κB signalling via disassociation of Keap1-Nrf2 in chondrocytes. Furthermore, NOM delays the disease progression in the mouse OA model. To sum up, this research indicated NOM possessed a new potential therapeutic option in osteoarthritis.
Insights
Nomilin (NOM) effectively reduces inflammation and cartilage degradation in osteoarthritis (OA) by suppressing key inflammatory pathways. This study highlights NOM as a promising therapeutic candidate for managing OA progression.
Area of Science:
- Biochemistry
- Pharmacology
- Immunology
Background:
- Osteoarthritis (OA) is a degenerative joint disorder characterized by cartilage erosion and inflammation.
- Triterpenoids, like nomilin (NOM), exhibit anti-inflammatory properties relevant to various diseases.
Purpose of the Study:
- To elucidate the therapeutic potential and underlying mechanisms of nomilin (NOM) in mitigating osteoarthritis (OA) progression.
- To investigate NOM's effects on inflammatory factors and extracellular matrix (ECM) degradation in OA models.
Main Methods:
- In vitro studies using chondrocytes stimulated with IL-1β.
- In vivo assessment in a mouse model of osteoarthritis.
- Analysis of inflammatory markers (NO, IL-6, PGE2, iNOS, TNF-α, COX-2) and ECM degradation.
- Investigation of the NF-κB signaling pathway and Keap1-Nrf2 interaction.
Main Results:
- NOM pre-treatment suppressed IL-1β-induced pro-inflammatory factors and ECM degradation in chondrocytes.
- NOM inhibited NF-κB signaling by disrupting the Keap1-Nrf2 complex in chondrocytes.
- NOM administration demonstrated a protective effect, delaying disease progression in a mouse OA model.
Conclusions:
- Nomilin (NOM) exhibits significant anti-inflammatory and chondroprotective effects relevant to osteoarthritis.
- NOM's mechanism involves the suppression of NF-κB signaling via the Keap1-Nrf2 pathway.
- NOM represents a potential novel therapeutic agent for osteoarthritis treatment.
