ArticleScientific reports2020
C-phycocyanin attenuates RANKL-induced osteoclastogenesis and bone resorption in vitro through inhibiting ROS levels, NFATc1 and NF-κB activation.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 45 citations in OpenAlex.
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- Shaping Orthodontics of the Future: Concepts and Implications from a Cellular and Molecular Perspective.International journal of molecular sciences · 2025Review
- Binary curcuminoid complex CRE-Bin inhibits osteoclast differentiation by suppressing the canonical NF-κB signaling pathway and modulating microRNA-223 expression.Scientific reports · 2025Article
- Development and synthesis of diffractaic acid analogs as potent inhibitors of colorectal cancer stem cell traits.Scientific reports · 2025Article
- Exploring the potential mechanism of B-phycoerythrin on DSS-induced colitis and colitis-associated bone loss based on network pharmacology, molecular docking, and experimental validation.Scientific reports · 2025Article
- Mitochondrial Transplantation: A Paradigm Shift in Osteoporosis Therapy.International journal of nanomedicine · 2025Review
- Stephanine Protects Against Osteoporosis by Suppressing Osteoclastogenesis via Inhibition of the RANKL-RANK Interaction.Journal of cellular and molecular medicine · 2024Article
- Compound Microalgae-Type Biofunctional Hydrogel for Wound Repair during Full-Thickness Skin Injuries.Polymers · 2024Article
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- Elucidation of Antiviral and Antioxidant Potential of C-Phycocyanin against HIV-1 Infection throughAntioxidants (Basel, Switzerland) · 2022Article
- Phycocyanin inhibitsAnnals of translational medicine · 2022Article
- L-Plastin Phosphorylation: Possible Regulation by a TNFR1 Signaling Cascade in Osteoclasts.Cells · 2021Article
- Induction of osteoclast formation by LOX mutant (LOXG473A) through regulation of autophagy.Annals of translational medicine · 2021Article
- Lipopolysaccharide- TLR-4 Axis regulates Osteoclastogenesis independent of RANKL/RANK signaling.BMC immunology · 2021Article
- Methylsulfonylmethane Increases the Alveolar Bone Density of Mandibles in Aging Female Mice.Frontiers in physiology · 2021Article
- Light Energy Dose and Photosensitizer Concentration Are Determinants of Effective Photo-Killing against Caries-Related Biofilms.International journal of molecular sciences · 2020Article
- Anti-inflammatory Activity of Bioactive Compounds from Microalgae and Cyanobacteria by Focusing on the Mechanisms of Action.Molecular biology reports · 2020Review
- Article
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Authors and funding
5 authors at 1 institution in 2 countries.
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Abstract
Excessive bone loss occurs in inflammatory disorders such as periodontitis and osteoporosis. The underlying mechanism is related to the differentiation of macrophages into multinucleated giant osteoclasts and their bone resorptive activity. C-Phycocyanin (C-PC) is a phycobiliprotein extracted from the blue-green algae, which has been shown to have various pharmacological effects. The role of C-PC on bone metabolism needs revelation. In this study, we determined the effectiveness of C-PC as an inhibitor of osteoclast differentiation, activity, and survival in vitro. We found that C-PC strongly inhibited the differentiation of macrophages to TRAP-positive osteoclasts, distinctive osteoclast specific podosomal organization, and dentine matrix resorption without any cytotoxicity. Also, it suppressed the expression of osteoclast specific markers, such as cathepsin K and integrin β3 at mRNA and protein levels. RANKL mediated signaling utilizes reactive oxygen species (ROS) for the differentiation of osteoclasts. C-PC attenuated RANKL stimulated ROS. Mechanistic studies indicate that C-PC has the potential to reduce osteoclast formation via blocking the degradation of cytosolic IκB-α and hence, the activation of downstream markers such as c-Fos and NFATc1. However, it does not have any effect on osteoblast-mediated bone formation in vitro. Collectively, our data suggest that C-PC may be utilized as a therapeutic agent that can target bone loss mediated by excessive osteoclastic bone resorption without affecting osteoblastic activity in bone.
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