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Buchumschlag von Cyanidin Chloride inhibits ovariectomy‐induced osteoporosis by suppressing RANKL‐mediated osteoclastogenesis and associated signaling pathways
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Cyanidin Chloride inhibits ovariectomy‐induced osteoporosis by suppressing RANKL‐mediated osteoclastogenesis and associated signaling pathways

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Zeitschriftentitel: Journal of Cellular Physiology
Personen und Körperschaften: Cheng, Jianwen, Zhou, Lin, Liu, Qian, Tickner, Jennifer, Tan, Zhen, Li, Xiaofeng, Liu, Mei, Lin, Xixi, Wang, Tao, Pavlos, Nathan J., Zhao, Jinmin, Xu, Jiake
In: Journal of Cellular Physiology, 233, 2018, 3, S. 2502-2512
Medientyp: E-Article
Sprache: Englisch
veröffentlicht:
Wiley
Schlagwörter:
Cell Biology
Clinical Biochemistry
Physiology
Details
Zusammenfassung: <jats:sec><jats:label /><jats:p>Over‐production and activation of osteoclasts is a common feature of osteolytic conditions such as osteoporosis, tumor‐associated osteolysis, and inflammatory bone erosion. Cyanidin Chloride, a subclass of anthocyanin, displays antioxidant and anti‐carcinogenesis properties, but its role in osteoclastic bone resorption and osteoporosis is not well understood. In this study, we showed that Cyanidin Chloride inhibits osteoclast formation, hydroxyapatite resorption, and receptor activator of NF‐κB ligand (RANKL)‐induced osteoclast marker gene expression; including <jats:italic>ctr</jats:italic>, <jats:italic>ctsk</jats:italic>, and <jats:italic>trap</jats:italic>. Further investigation revealed that Cyanidin Chloride inhibits RANKL‐induced NF‐κB activation, suppresses the degradation of IκB‐α and attenuates the phosphorylation of extracellular signal‐regulated kinases (ERK). In addition, Cyanidin Chloride abrogated RANKL‐induced calcium oscillations, the activation of nuclear factor of activated T cells calcineurin‐dependent 1 (NFATc1), and the expression of c‐Fos. Further, we showed that Cyanidin Chloride protects against ovariectomy‐induced bone loss in vivo. Together our findings suggest that Cyanidin Chloride is capable of inhibiting osteoclast formation, hydroxyapatite resorption and RANKL‐induced signal pathways in vitro and OVX‐induced bone loss in vivo, and thus might have therapeutic potential for osteolytic diseases.</jats:p></jats:sec>
Umfang: 2502-2512
ISSN: 0021-9541
1097-4652
DOI: 10.1002/jcp.26126