2. Academic Validation
  3. Dioscin inhibits osteoclast differentiation and bone resorption though down-regulating the Akt signaling cascades

Dioscin inhibits osteoclast differentiation and bone resorption though down-regulating the Akt signaling cascades

  • Biochem Biophys Res Commun. 2014 Jan 10;443(2):658-65. doi: 10.1016/j.bbrc.2013.12.029.
Xinhua Qu 1,  Zanjing Zhai 1,  Xuqiang Liu 1,  Haowei Li 1,  Zhengxiao Ouyang 2,  Chuanlong Wu 1,  Guangwang Liu 3,  Qiming Fan 1,  Tingting Tang 1,  An Qin 4,  Kerong Dai 5
Affiliations

Affiliations

  • 1 Shanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • 2 Shanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Orthopaedics, Hunan Provincial Tumor Hospital and Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
  • 3 Department of Orthopaedic Surgery, The Central Hospital of Xuzhou, Affiliated Hospital of Medical Collage of Southeast University, Xuzhou, China.
  • 4 Shanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: dr.qinan@gmail.com.
  • 5 Shanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: krdai@163.com.
PMID: 24333429 DOI: 10.1016/j.bbrc.2013.12.029
Abstract

Bone resorption is the unique function of osteoclasts (OCs) and is critical for both bone homeostasis and pathologic bone diseases including osteoporosis, rheumatoid arthritis and tumor bone metastasis. Thus, searching for natural compounds that may suppress osteoclast formation and/or function is promising for the treatment of osteoclast-related diseases. In this study, we for the first time demonstrated that dioscin suppressed RANKL-mediated osteoclast differentiation and bone resorption in vitro in a dose-dependent manner. The suppressive effect of dioscin is supported by the reduced expression of osteoclast-specific markers. Further molecular analysis revealed that dioscin abrogated Akt phosphorylation, which subsequently impaired RANKL-induced nuclear factor-kappaB (NF-κB) signaling pathway and inhibited NFATc1 transcriptional activity. Moreover, in vivo studies further verified the bone protection activity of dioscin in osteolytic animal model. Together our data demonstrate that dioscin suppressed RANKL-induced osteoclast formation and function through Akt signaling cascades. Therefore, dioscin is a potential natural agent for the treatment of osteoclast-related diseases.

Keywords

AKT cascades; Dioscin; Osteoclast; Osteolysis.

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