ArticleJournal of orthopaedic surgery and research2024
Astaxanthin-mediated Nrf2 activation ameliorates glucocorticoid-induced oxidative stress and mitochondrial dysfunction and impaired bone formation of glucocorticoid-induced osteonecrosis of the femoral head in rats.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Alpha-2-macroglobulin attenuates glucocorticoid-induced osteonecrosis of the femoral head by enhancing osteogenesis and antioxidant defense via the Akt/Nrf2 signaling pathway.Journal of molecular histology · 2026Article
- Exploring the Multifunctional Benefits of Astaxanthin in Aging, Oxidative Stress, Immune Dysfunction, Gut and Skin Health.Antioxidants (Basel, Switzerland) · 2026Review
- Mechanistic and Therapeutic Insights into Nrf2-Mediated Redox Regulation in Periodontitis.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Therapeutic Management of Glucocorticoid-Induced Osteoporosis with a Focus on Older Adults: A Narrative Review.Drugs & aging · 2026Review
- New insights into the mechanism of microvascular rarefaction via endothelial-mesenchymal transition in steroid-induced osteonecrosis of femoral head.Scientific reports · 2025Article
- Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes.Redox report : communications in free radical research · 2025Review
- Human Umbilical Cord Mesenchymal Stem Cells Prevent Steroid-Induced Avascular Necrosis of the Femoral Head by Modulating Cellular Autophagy.Biomedicines · 2024Article
- Invited Perspective: New Insight into Cadmium-Related Osteoporosis Yields Hope for Prevention and Therapy.Environmental health perspectives · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundOsteonecrosis of the femoral head caused by glucocorticoids (GIONFH) is a significant issue resulting from prolonged or excessive clinical glucocorticoid use. Astaxanthin, an orange-red carotenoid present in marine organisms, has been the focus of this study to explore its impact and mechanism on osteoblast apoptosis induced by dexamethasone (Dex) and GIONFH.
methodsIn this experiment, bioinformatic prediction, molecular docking and dynamics simulation, cytotoxicity assay, osteogenic differentiation, qRT-PCR analysis, terminal uridine nickend labeling (TUNEL) assay, determination of intracellular ROS, mitochondrial function assay, immunofluorescence, GIONFH rat model construction, micro-computed tomography (micro-CT) scans were performed.
resultsOur research demonstrated that a low dose of astaxanthin was non-toxic to healthy osteoblasts and restored the osteogenic function of Dex-treated osteoblasts by reducing oxidative stress, mitochondrial dysfunction, and apoptosis. Furthermore, astaxanthin rescued the dysfunction in poor bone quality, bone metabolism and angiogenesis of GIONFH rats. The mechanism behind this involves astaxanthin counteracting Dex-induced osteogenic damage by activating the Nrf2 pathway.
conclusionAstaxanthin shields osteoblasts from glucocorticoid-induced oxidative stress and mitochondrial dysfunction via Nrf2 pathway activation, making it a potential therapeutic agent for GIONFH treatment.
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