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Euphorbia factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast

Title
Euphorbia factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast
Authors
Hong S.-E.Lee J.Seo D.-H.In Lee H.Ri Park D.Lee G.-R.Jo Y.-J.Kim N.Kwon M.Shon H.Kyoung Seo E.Kim H.-S.Young Lee S.Jeong W.
Ewha Authors
이수영서은경정우진
SCOPUS Author ID
이수영scopus; 서은경scopus; 정우진scopus; 서은경scopus
Issue Date
2017
Journal Title
Free Radical Biology and Medicine
ISSN
0891-5849JCR Link
Citation
vol. 112, pp. 191 - 199
Keywords
ApoptosisBone resorptionOsteoclastReactive oxygen species
Publisher
Elsevier Inc.
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Excessive bone resorption caused by increased osteoclast number or activity leads to a variety of bone diseases including osteoporosis, rheumatoid arthritis and periodontitis. Thus, the therapeutic strategy for these diseases has been focused primarily on the inhibition of osteoclast formation and function. This study shows that euphorbia factor L1 (EFL1), a diterpenoid isolated from Euphorbia lathyris, inhibited osteoclastogenesis and induced osteoclast apoptosis. EFL1 suppressed osteoclast formation and bone resorption at both initial and terminal differentiation stages. EFL1 inhibited receptor activator of NF-κB ligand (RANKL)-induced NFATc1 induction with attenuated NF-κB activation and c-Fos expression. EFL1 decreased the level of reactive oxygen species by scavenging them or activating Nrf2, and inhibited PGC-1β that regulates mitochondria biogenesis. In addition, EFL1 induced apoptosis in differentiated osteoclasts by increasing Fas ligand expression followed by caspase activation. Moreover, EFL1 inhibited inflammation-induced bone erosion and ovariectomy-induced bone loss in mice. These findings suggest that EFL1 inhibits osteoclast differentiation by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast, and may provide therapeutic potential for preventing or treating bone-related diseases caused by excessive osteoclast. © 2017
DOI
10.1016/j.freeradbiomed.2017.07.030
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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