IADR Abstract Archives
C-Phycocyanin Attenuates Osteoclastogenesis And Bone Resorption In Vitro
Objectives: 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 in bone metabolism needs further elucidation. In this study, we tested the effect of C-PC on osteoclast differentiation, activity, and survival in vitro.
Methods: Murine osteoclasts were generated from RAW 264.7 cells. We did the following tests to obtain our results: MTT assay, TRAP staining, actin staining, bone resorption assay, ROS analysis, immunoblotting analysis, RT-PCR, Alizarin red staining, and Alkaline phosphatase (ALP) activity assay. Quantitative data are all expressed as mean ± SD and statistical significance was determined using one - way ANOVA or Student T-test when applicable (Graph Pad Inc, San Diego, CA). The level of significance was set at P < 0.05.
Results: C-PC strongly inhibited the differentiation of macrophages to TRAP-positive osteoclasts, typical osteoclast specific podosomal organization, and bone resorption without any cytotoxicity. The protein and mRNA expression of osteoclast specific markers, such as cathepsin K and integrin β3 were suppressed by C-PC. Reactive oxygen species (ROS) can activate osteoclasts, and C-PC has the potential to attenuate this effect. Furthermore, C-PC has the potential to reduce osteoclast formation via blocking the degradation of cytosolic IκBα 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.
Conclusions: Collectively, our data suggest that C-PC may be utilized as a preventive or therapeutic agent that can target bone lesions characterized by excessive osteoclastic bone loss.
Methods: Murine osteoclasts were generated from RAW 264.7 cells. We did the following tests to obtain our results: MTT assay, TRAP staining, actin staining, bone resorption assay, ROS analysis, immunoblotting analysis, RT-PCR, Alizarin red staining, and Alkaline phosphatase (ALP) activity assay. Quantitative data are all expressed as mean ± SD and statistical significance was determined using one - way ANOVA or Student T-test when applicable (Graph Pad Inc, San Diego, CA). The level of significance was set at P < 0.05.
Results: C-PC strongly inhibited the differentiation of macrophages to TRAP-positive osteoclasts, typical osteoclast specific podosomal organization, and bone resorption without any cytotoxicity. The protein and mRNA expression of osteoclast specific markers, such as cathepsin K and integrin β3 were suppressed by C-PC. Reactive oxygen species (ROS) can activate osteoclasts, and C-PC has the potential to attenuate this effect. Furthermore, C-PC has the potential to reduce osteoclast formation via blocking the degradation of cytosolic IκBα 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.
Conclusions: Collectively, our data suggest that C-PC may be utilized as a preventive or therapeutic agent that can target bone lesions characterized by excessive osteoclastic bone loss.