Cyanidin chloride inhibits ovariectomy-induced osteoporosis by suppressing RANKL-mediated osteoclastogenesis and associated signaling pathways

1:57 pm 15 Dec 2017

First published: 7 September 2017


The authors acknowledge the facilities, and the scientific and technical assistance of the National Imaging Facility at the Center for Microscopy, Characterization & Analysis, the University of Western Australia, a facility funded by the University, State and Commonwealth Governments. This study was supported in part by the National Health and Medical Research Council of Australia. This study was also supported by grants from the National Natural Science Foundation of China


Jianwen Cheng, Lin Zhou, Qian Liu, Jennifer Tickner, Zhen Tan, Xiaofeng Li, Mei Liu, Xixi Lin, Tao Wang, Nathan J. Pavlos, Jinmin Zhao, Jiake Xu

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 ctr, ctsk, and trap. 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.

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