ArticleInternational journal of molecular sciences2023
The Triterpenoid Nrf2 Activator, CDDO-Me, Decreases Neutrophil Senescence in a Murine Model of Joint Damage.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Synthesis and Antitumor Potency of 2International journal of molecular sciences · 2026Article
- Natural products and immune-cell responses in osteoarthritis: mechanisms, evidence maturity, and translational gaps.Frontiers in immunology · 2026Review
- Mechanism of Neutrophil p90RSK-Nrf2 Signaling Pathway in Atherosclerosis.Balkan medical journal · 2025Article
- Immunosenescence in Sepsis: Molecular Mechanisms and Potential Therapeutic Targets.Aging and disease · 2025Review
- Nrf2-dependent effects of CDDO-Me on bactericidal activity in macrophage infection models.Frontiers in immunology · 2025Article
- Article
- Advancing osteoarthritis therapy with GMOCS hydrogel-loaded BMSCs-exos.Journal of nanobiotechnology · 2024Article
- Development of Potential Therapeutic Agents from Black Elderberries (the Fruits ofMolecules (Basel, Switzerland) · 2024Review
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
The synthetic 2-cyano-3,12-dioxo-oleana-1,9(11)-dien-28-oic acid methyl ester (CDDO-Me) is a potent activator of the erythroid 2-p45-derived factor 2, Nrf2, a leucine-zipper regulator of the antioxidant response. Herein, we investigated the effect of CDDO-Me on neutrophil function in a murine model of joint damage. Collagenase-induced osteoarthritis (CIOA) was initiated by the intra-articular injection of collagenase in the knee-joint cavity of Balb/c mice. CDDO-Me was administrated intra-articularly twice a week starting at day 7 post-CIOA, and its effect was evaluated at day 14. Neutrophils in blood and bone marrow (BM), cell apoptosis, necrosis, expression of C-X-C chemokine receptor 4 (CXCR4), beta-galactosidase (β-Gal), and Nrf2 levels were measured by flow cytometry. In vitro, CDDO-Me promoted cell survival, reduced cell necrosis, and increased Nrf2 levels by 1.6 times. It decreased surface CXCR4 expression and reduced the frequency of senescent β-Gal+CXCR4+ neutrophils by three times. In vivo, the degree of knee-joint damage in CIOA was correlated with upregulated CXCR4 on CD11b+ neutrophils. CDDO-Me improved the disease histological score, increased the levels of Nrf2, and downregulated surface CXCR4 on mature BM cells. Our data suggest that CDDO-Me may act as a potent regulator of neutrophil senescence during the progression of knee-joint damage.
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Registered trials
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