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Your search keyword '"inflammatory bone destruction"' showing total 2 results
Start Over Descriptor "inflammatory bone destruction" Journal theranostics
2 results on '"inflammatory bone destruction"'

1. Gold Clusters Prevent Inflammation-Induced Bone Erosion through Inhibiting the Activation of NF-κB Pathway

Author

Kaixiao Hou, Xiangchun Zhang, Pengju Cai, Qing Yuan, Yawen Yao, Fuping Gao, Xueyun Gao, Jinling Yuan, Liang Gao, and Xiaojun Ren

Subjects
Male, Medicine (miscellaneous), Osteoclasts, Inflammation, 02 engineering and technology, 010402 general chemistry, 01 natural sciences, gold cluster, Proinflammatory cytokine, Cell Line, chemistry.chemical_compound, Mice, Osteoclast, In vivo, Osteogenesis, medicine, Animals, inflammatory bone destruction, Bone Resorption, Receptor, Pharmacology, Toxicology and Pharmaceutics (miscellaneous), osteoclastogenesis, Periodontitis, NF-κB pathway, biology, Chemistry, Macrophages, RANK Ligand, NF-kappa B, NF-κB, Cell Differentiation, 021001 nanoscience & nanotechnology, medicine.disease, 0104 chemical sciences, medicine.anatomical_structure, RAW 264.7 Cells, RANKL, biology.protein, Cancer research, Gold, medicine.symptom, 0210 nano-technology, Research Paper, Signal Transduction
Abstract

Inflammation-induced bone erosion is a major pathological factor in several chronic inflammatory diseases that often cause severe outcomes, such as rheumatoid arthritis and periodontitis. Plenty of evidences indicated that the inflammatory bone destruction was attributed to an increase in the number of bone-resorbing osteoclasts. However, anti-resorptive therapy alone failed to prevent bone loss in an inflammatory condition. Conventional anti-inflammation treatments are usually intended to suppress inflammation only, but ignore debilitating the subsequent bone destruction. Therefore, inhibition of proinflammatory activation of osteoclastogenesis could be an important strategy for the development of drugs aimed at preventing inflammatory bone destruction. Methods: In this study, we synthesized a peptide coated gold cluster to evaluate its effects on inflammatory osteoclastogenesis in vitro and inflammation-induced bone destruction in vivo. The in vitro anti-inflammation and anti-osteoclastogenesis effects of the cluster were evaluated in LPS-stimulated and receptor activator of nuclear factor κB ligand (RANKL) stimulated macrophages, respectively. The LPS-induced expression of crucial pro-inflammation cytokines and RANKL-induced osteoclastogenesis as well as the activation of NF-κB pathway in both situations were detected. The inflammation-induced RANKL expression and subsequent inflammatory bone destruction in vivo were determined in collagen-immunized mice. Results: The gold cluster strongly suppresses RANKL-induced osteoclast formation via inhibiting the activation of NF-κB pathway in vitro. Moreover, treatment with the clusters at a dose of 5 mg Au/kg.bw significantly reduces the severity of inflammation-induced bone and cartilage destruction in vivo without any significant toxicity effects. Conclusion: Therefore, the gold clusters may offer a novel potent therapeutic stratagem for inhibiting chronic inflammation associated bone destruction.

Published
2019

2. Gold Clusters Prevent Inflammation-Induced Bone Erosion through Inhibiting the Activation of NF-κB Pathway.

Author

Yuan Q, Gao F, Yao Y, Cai P, Zhang X, Yuan J, Hou K, Gao L, Ren X, and Gao X

Subjects
Animals, Bone Resorption drug therapy, Bone Resorption metabolism, Cell Differentiation drug effects, Cell Line, Inflammation metabolism, Macrophages drug effects, Macrophages metabolism, Male, Mice, Osteoclasts drug effects, Osteoclasts metabolism, Osteogenesis drug effects, RANK Ligand metabolism, RAW 264.7 Cells, Gold administration & dosage, Gold chemistry, Inflammation drug therapy, NF-kappa B metabolism, Signal Transduction drug effects
Abstract

Inflammation-induced bone erosion is a major pathological factor in several chronic inflammatory diseases that often cause severe outcomes, such as rheumatoid arthritis and periodontitis. Plenty of evidences indicated that the inflammatory bone destruction was attributed to an increase in the number of bone-resorbing osteoclasts. However, anti-resorptive therapy alone failed to prevent bone loss in an inflammatory condition. Conventional anti-inflammation treatments are usually intended to suppress inflammation only, but ignore debilitating the subsequent bone destruction. Therefore, inhibition of proinflammatory activation of osteoclastogenesis could be an important strategy for the development of drugs aimed at preventing inflammatory bone destruction. Methods: In this study, we synthesized a peptide coated gold cluster to evaluate its effects on inflammatory osteoclastogenesis in vitro and inflammation-induced bone destruction in vivo . The in vitro anti-inflammation and anti-osteoclastogenesis effects of the cluster were evaluated in LPS-stimulated and receptor activator of nuclear factor κB ligand (RANKL) stimulated macrophages, respectively. The LPS-induced expression of crucial pro-inflammation cytokines and RANKL-induced osteoclastogenesis as well as the activation of NF-κB pathway in both situations were detected. The inflammation-induced RANKL expression and subsequent inflammatory bone destruction in vivo were determined in collagen-immunized mice. Results: The gold cluster strongly suppresses RANKL-induced osteoclast formation via inhibiting the activation of NF-κB pathway in vitro . Moreover, treatment with the clusters at a dose of 5 mg Au/kg.bw significantly reduces the severity of inflammation-induced bone and cartilage destruction in vivo without any significant toxicity effects. Conclusion: Therefore, the gold clusters may offer a novel potent therapeutic stratagem for inhibiting chronic inflammation associated bone destruction., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.

Published
2019
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