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Platycodin D Inhibits Osteoclastogenesis by Repressing the NFATc1 and MAPK Signaling Pathway
Author(s) -
Choi Jae Ho,
Han Younho,
Kim Yong An,
Jin Sun Woo,
Lee Gi Ho,
Jeong Hyung Min,
Lee Hyun Sun,
Chung Young Chul,
Lee Young Chun,
Kim Eun Ju,
Lee Kwang Youl,
Jeong Hye Gwang
Publication year - 2017
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25763
Subject(s) - rankl , osteoclast , chemistry , mapk/erk pathway , p38 mitogen activated protein kinases , activator (genetics) , bone remodeling , bone resorption , microbiology and biotechnology , receptor , endocrinology , pharmacology , medicine , signal transduction , biochemistry , biology
Platycodon grandiflorum root‐derived saponins (Changkil saponins, CKS) are reported to have many pharmacological activities. In our latest research, CKS was proven to have a significant osteogenic effect. However, the detail molecular mechanism of CKS on osteoclastic differentiation has not been fully investigated. Administration of CKS considerably reduced OVX‐induced bone loss, and ameliorated the reduction in plasma levels of alkaline phosphatase, calcium, and phosphorus observed in OVX mice. CKS also repressed the deterioration of bone trabecular microarchitecture. Interestingly, platycodin D, the most abundant and major pharmacological constituent of triterpenoid CKS, inhibited receptor activator of NF‐κB ligand (RANKL)‐induced activation of NF‐κB, and ERK and p38 MAPK, ultimately repressing osteoclast differentiation. OVX‐induced bone turnover was attenuated by CKS, possibly via repression of osteoclast differentiation by platycodin D, the active component of CKS. Platycodin D can be regarded as an antiosteoporotic candidate for treatment of osteoporosis diseases. J. Cell. Biochem. 118: 860–868, 2017. © 2016 Wiley Periodicals, Inc.