2. Academic Validation
  3. Cyanidin Chloride inhibits ovariectomy-induced osteoporosis by suppressing RANKL-mediated osteoclastogenesis and associated signaling pathways

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

  • J Cell Physiol. 2018 Mar;233(3):2502-2512. doi: 10.1002/jcp.26126.
Jianwen Cheng 1 2 3,  Lin Zhou 3,  Qian Liu 1,  Jennifer Tickner 3,  Zhen Tan 1 2,  Xiaofeng Li 1 2,  Mei Liu 4,  Xixi Lin 1,  Tao Wang 1,  Nathan J Pavlos 5,  Jinmin Zhao 1 2 6,  Jiake Xu 1 3
Affiliations

Affiliations

  • 1 Research Center for Regenerative Medicine, and Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Guangxi, China.
  • 2 Department of Orthopaedic Surgery, the First Affiliated Hospital of Guangxi Medical University, Guangxi, China.
  • 3 School of Pathology and Laboratory Medicine, The University of Western Australia, Perth, Western Australia, Australia.
  • 4 Jiangsu Key Laboratory for Molecular and Medical Biotechnology and College of Life Sciences, Nanjing Normal University, Nanjing, China.
  • 5 School of Surgery, The University of Western Australia, Perth, Western Australia, Australia.
  • 6 Guangxi Collaborative Innovation Center for Biomedicine, Guangxi Medical University, Guangxi, China.
PMID: 28771720 DOI: 10.1002/jcp.26126
Abstract

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.

Keywords

Cyanidin Chloride; RANKL; bone resorption; osteoclast; osteolysis.

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