4.6 Article

Poria cocos polysaccharide attenuates RANKL-induced osteoclastogenesis by suppressing NFATc1 activity and phosphorylation of ERK and STAT3

期刊

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 647, 期 -, 页码 76-83

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2018.04.011

关键词

Poria cocos polysaccharide; Osteoclast; Bone resorption; MAPK; STAT3

资金

  1. Nature Science Foundation of China [81572164]
  2. National Key Technology Research and Development Program of China [2017YFC1103300]
  3. Guangxi Natural Science Foundation [2016GXNSFAA380295]
  4. University Scientific Research Project of Guangxi Province [KY2015YB054]
  5. Nanning Scientific Research and Technology Development Plan [20123142]
  6. Guangxi Scientific Research and Technology Development Plan Project [GKG13349003, 1598013-15]
  7. Western Australia Medical & Health Research Infrastructure Fund
  8. Arthritis Australia foundation
  9. University of Western Australia (UWA) Research Collaboration Awards
  10. Australian Health and Medical Research Council (NHMRC) [1107828, 1027932]

向作者/读者索取更多资源

Pathological fractures caused by osteolytic lesions seriously threaten the health of patients. Osteoclasts play important roles in bone resorption whose hyperfunction are closely related to osteolytic lesions. Studies on osteoclast differentiation and function assist in the prevention of excessive bone loss associated diseases. We screened a variety of natural compounds with anti-inflammatory effect and found that poria cocos polysaccharide (PCP) inhibited RANKL-induced osteoclast formation and bone resorption via TRAcP staining, immunofluorescence, RT-PCR and western blot. PCP down-regulated phosphorylation of STAT3, P38, ERK and JNK, and thus repressed the expression of NFAcT1 and c-Fos during RANKL-induced osteoclastogenesis. Besides, the expression of bone resorption related genes such as TRAcP and CTSK was suppressed by PCP. The results suggest that PCP can be invoked as a candidate for the treatment of osteolytic diseases by inhibiting osteoclastogenesis.

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