ArticleInternational journal of molecular sciences2018
Suppression Effect of Astaxanthin on Osteoclast Formation In Vitro and Bone Loss In Vivo.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 56 citations in OpenAlex.
- Mechanistic and Therapeutic Insights into Nrf2-Mediated Redox Regulation in Periodontitis.Antioxidants (Basel, Switzerland) · 2026Review
- Plant-derived food bioactives in bone health: from multi-targeted roles to molecular mechanisms in osteoporosis.Frontiers in nutrition · 2025Review
- Pharmacological mechanism of natural products to treat osteoporosis: a focus on the autophagy.Frontiers in pharmacology · 2025Review
- Anti-osteoporotic effects ofNutrition research and practice · 2024Article
- Processed microalgae: green gold for tissue regeneration and repair.Theranostics · 2024Review
- Metabolic bone disorders and the promise of marine osteoactive compounds.Cellular and molecular life sciences : CMLS · 2023Review
- Anti-Osteoporotic Potential of Water Extract ofNutrients · 2023Article
- Astaxanthin as a Potent Antioxidant for Promoting Bone Health: An Up-to-Date Review.Antioxidants (Basel, Switzerland) · 2023Review
- Ginsenoside Rc Promotes Bone Formation in Ovariectomy-Induced Osteoporosis In Vivo and Osteogenic Differentiation In Vitro.International journal of molecular sciences · 2022Article
- Targeting Sirt1, AMPK, Nrf2, CK2, and Soluble Guanylate Cyclase with Nutraceuticals: A Practical Strategy for Preserving Bone Mass.International journal of molecular sciences · 2022Review
- Development of Astaxanthin-Loaded Nanosized Liposomal Formulation to Improve Bone Health.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Mechanistic role of astaxanthin derived from shrimp against certain metabolic disorders.Food science & nutrition · 2022Review
- Inhibitory Effects of Astaxanthin on CML-HSA-Induced Inflammatory and RANKL-Induced Osteoclastogenic Gene Expression in RAW 264.7 Cells.Biomedicines · 2021Article
- Article
- Anti-Inflammatory and Anticancer Effects of Microalgal Carotenoids.Marine drugs · 2021Review
- Fucoxanthin Suppresses Osteoclastogenesis via Modulation of MAP Kinase and Nrf2 Signaling.Marine drugs · 2021Article
- Emerging Natural-Product-Based Treatments for the Management of Osteoarthritis.Antioxidants (Basel, Switzerland) · 2021Review
- Cyanobacteria and Microalgae as Sources of Functional Foods to Improve Human General and Oral Health.Molecules (Basel, Switzerland) · 2020Review
- The Beneficial Effect of Boswellic Acid on Bone Metabolism and Possible Mechanisms of Action in Experimental Osteoporosis.Nutrients · 2020Article
- Carotenoids and Periodontal Infection.Nutrients · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is characterized by a reduction of the bone mineral density (BMD) and microarchitectural deterioration of the bone, which lead to bone fragility and susceptibility to fracture. Astaxanthin (AST) has a variety of biological activities, such as a protective effect against asthma or neuroinflammation, antioxidant effect, and decrease of the osteoclast number in the right mandibles in the periodontitis model. Although treatment with AST is known to have an effect on inflammation, no studies on the effect of AST exposure on bone loss have been performed. Thus, in the present study, we examined the antiosteoporotic effect of AST on bone mass in ovariectomized (OVX) mice and its possible mechanism of action. The administration of AST (5, 10 mg/kg) for 6 weeks suppressed the enhancement of serum calcium, inorganic phosphorus, alkaline phosphatase, total cholesterol, and tartrate-resistant acid phosphatase (TRAP) activity. The bone mineral density (BMD) and bone microarchitecture of the trabecular bone in the tibia and femur were recovered by AST exposure. Moreover, in the in vitro experiment, we demonstrated that AST inhibits osteoclast formation through the expression of the nuclear factor of activated T cells (NFAT) c1, dendritic cell-specific transmembrane protein (DC-STAMP), TRAP, and cathepsin K without any cytotoxic effects on bone marrow-derived macrophages (BMMs). Therefore, we suggest that AST may have therapeutic potential for the treatment of postmenopausal osteoporosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.