2. Academic Validation
  3. Gentiopicroside inhibits RANKL-induced osteoclastogenesis by regulating NF-κB and JNK signaling pathways

Gentiopicroside inhibits RANKL-induced osteoclastogenesis by regulating NF-κB and JNK signaling pathways

  • Biomed Pharmacother. 2018 Apr;100:142-146. doi: 10.1016/j.biopha.2018.02.014.
Fangqing Chen 1,  Lin Xie 2,  Ran Kang 2,  Rongrong Deng 2,  Zhipeng Xi 2,  Daoxi Sun 2,  Jin Zhu 3,  Liming Wang 4
Affiliations

Affiliations

  • 1 The Third Clinical Medical College, Nanjing Medical University, Nanjing 210029, China; Department of Orthopedics, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China.
  • 2 Department of Orthopedics, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China.
  • 3 School of Basic Medicine, Nanjing Medical University, Nanjing 210029, China. Electronic address: [email protected].
  • 4 The Third Clinical Medical College, Nanjing Medical University, Nanjing 210029, China; Department of Orthopedics, The Affiliated Nanjing Hospital of Nanjing Medical University, Nanjing 210006, China. Electronic address: [email protected].
PMID: 29428661 DOI: 10.1016/j.biopha.2018.02.014
Abstract

Gentiopicroside, a main active component from the traditional Chinese herb medicine Gentiana manshurica Kitag, has been shown to possess anti-arthritis effect. However, the molecular mechanism of gentiopicroside on the osteoclast formation remains unclear. The present study was designed to investigate the effects and mechanisms of gentiopicroside on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. The results showed that pre-treatment with gentiopicroside significantly inhibited RANKL-induced osteoclast formation from mouse bone marrow macrophages (BMMs). In addition, we observed that gentiopicroside efficiently suppressed osteoclastogenesis-related marker genes expression in RANKL-stimulated BMMs. Mechanistically, gentiopicroside suppressed RANKL-induced the activation of JNK and NF-κB signaling pathways in BMMs. Taken together, the present study demonstrated that gentiopicroside inhibits RANKL-induced osteoclastogenesis through the inactivation of JNK and NF-κB signaling pathways. Thus, gentiopicroside may be a promising agent for the treatment of osteoporosis.

Keywords

Gentiopicroside; JNK pathway; NF-κB pathway; Osteoporosis; RANKL.

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