Article Publish Status: FREE
Abstract Title:

Poncirin Inhibits Osteoclast Differentiation and Bone Loss through Down-Regulation of NFATc1and.

Abstract Source:

Biomol Ther (Seoul). 2020 Jul 1 ;28(4):337-343. PMID: 31500404

Abstract Author(s):

Kwang-Hoon Chun, Hyun Chul Jin, Ki Sung Kang, Tong-Shin Chang, Gwi Seo Hwang

Article Affiliation:

Kwang-Hoon Chun


Activation of osteoclast and inactivation of osteoblast result in loss of bone mass with bone resorption, leading to the pathological progression of osteoporosis. The receptor activator of NF-κB ligand (RANKL) is a member of the TNF superfamily, and is a key mediator of osteoclast differentiation. A flavanone glycoside isolated from the fruit of, poncirin has anti-allergic, hypocholesterolemic, anti-inflammatory and anti-platelet activities. The present study investigates the effect of poncirin on osteoclast differentiation of RANKL-stimulated RAW264.7 cells. We observed reduced formation of RANKL-stimulated TRAP-positive multinucleated cells (a morphological feature of osteoclasts) after poncirin exposure. Real-time qPCR analysis showed suppression of the RANKL-mediated induction of key osteoclastogenic molecules such as NFATc1, TRAP, c-Fos, MMP9 and cathepsin K after poncirin treatment. Poncirin also inhibited the RANKL-mediated activation of NF-κB and, notably, JNK, without changes in ERK and p38 expression in RAW264.7 cells. Furthermore, we assessed theefficacy of poncirin in the lipopolysaccharide (LPS)-induced bone erosion model. Evaluating the micro-CT of femurs revealed that bone erosion in poncirin treated mice was markedly attenuated. Our results indicate that poncirin exerts anti-osteoclastic effectsandby suppressing osteoclast differentiation. We believe that poncirin is a promising candidate for inflammatory bone loss therapeutics.

Study Type : Animal Study, In Vitro Study
Additional Links
Pharmacological Actions : Osteoprotective : CK(971) : AC(351)

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