luteolin-7-glucoside and Osteolysis

luteolin-7-glucoside has been researched along with Osteolysis* in 1 studies

Other Studies

1 other study(ies) available for luteolin-7-glucoside and Osteolysis

Article	Year
Luteoloside prevents lipopolysaccharide-induced osteolysis and suppresses RANKL-induced osteoclastogenesis through attenuating RANKL signaling cascades. Journal of cellular physiology, 2018, Volume: 233, Issue:2 Bone destruction or osteolysis marked by excessive osteoclastic bone resorption is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions such as periprosthetic joint infection and periprosthetic loosening. Luteoloside, a flavonoid, is a natural bioactive compound with anti-inflammation and anti-tumor properties. However, the effect of Luteoloside on inflammation-induced osteolysis is unknown. Here, we found that Luteoloside exhibited a strong inhibitory effect on lipopolysaccharide (LPS)-induced osteolysis in vivo. In addition, Luteoloside suppressed RANKL-induced osteoclast differentiation and abrogated bone resorption in a dose-dependent manner. Further, we found that the anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca Topics: Animals; Anti-Inflammatory Agents; Calcium Signaling; Disease Models, Animal; Dose-Response Relationship, Drug; Durapatite; Glucosides; Lipopolysaccharides; Luteolin; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinases; NF-kappa B; NFATC Transcription Factors; Osteoclasts; Osteogenesis; Osteolysis; RANK Ligand; RAW 264.7 Cells; Skull; Time Factors	2018

Article

Year

Luteoloside prevents lipopolysaccharide-induced osteolysis and suppresses RANKL-induced osteoclastogenesis through attenuating RANKL signaling cascades.

Journal of cellular physiology, 2018, Volume: 233, Issue:2

Bone destruction or osteolysis marked by excessive osteoclastic bone resorption is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions such as periprosthetic joint infection and periprosthetic loosening. Luteoloside, a flavonoid, is a natural bioactive compound with anti-inflammation and anti-tumor properties. However, the effect of Luteoloside on inflammation-induced osteolysis is unknown. Here, we found that Luteoloside exhibited a strong inhibitory effect on lipopolysaccharide (LPS)-induced osteolysis in vivo. In addition, Luteoloside suppressed RANKL-induced osteoclast differentiation and abrogated bone resorption in a dose-dependent manner. Further, we found that the anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca

Topics: Animals; Anti-Inflammatory Agents; Calcium Signaling; Disease Models, Animal; Dose-Response Relationship, Drug; Durapatite; Glucosides; Lipopolysaccharides; Luteolin; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinases; NF-kappa B; NFATC Transcription Factors; Osteoclasts; Osteogenesis; Osteolysis; RANK Ligand; RAW 264.7 Cells; Skull; Time Factors

2018