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Euphorbia factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast.
Free Radic Biol Med. 2017 11; 112:191-199.FR

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.

Authors+Show Affiliations

Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Biomedical Engineering, College of Health Science, Institute of Medical Engineering, Yonsei University, Wonju, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.College of Pharmacy, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Biomedical Engineering, College of Health Science, Institute of Medical Engineering, Yonsei University, Wonju, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea.Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Republic of Korea. Electronic address: jeongw@ewha.ac.kr.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28774817

Citation

Hong, Seong-Eun, et al. "Euphorbia Factor L1 Inhibits Osteoclastogenesis By Regulating Cellular Redox Status and Induces Fas-mediated Apoptosis in Osteoclast." Free Radical Biology & Medicine, vol. 112, 2017, pp. 191-199.
Hong SE, Lee J, Seo DH, et al. Euphorbia factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast. Free Radic Biol Med. 2017;112:191-199.
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. (2017). Euphorbia factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast. Free Radical Biology & Medicine, 112, 191-199. https://doi.org/10.1016/j.freeradbiomed.2017.07.030
Hong SE, et al. Euphorbia Factor L1 Inhibits Osteoclastogenesis By Regulating Cellular Redox Status and Induces Fas-mediated Apoptosis in Osteoclast. Free Radic Biol Med. 2017;112:191-199. PubMed PMID: 28774817.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Euphorbia factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast. AU - Hong,Seong-Eun, AU - Lee,Jiae, AU - Seo,Dong-Hyun, AU - In Lee,Hye, AU - Ri Park,Doo, AU - Lee,Gong-Rak, AU - Jo,You-Jin, AU - Kim,Narae, AU - Kwon,Minjung, AU - Shon,Hansem, AU - Kyoung Seo,Eun, AU - Kim,Han-Sung, AU - Young Lee,Soo, AU - Jeong,Woojin, Y1 - 2017/07/31/ PY - 2017/02/10/received PY - 2017/07/11/revised PY - 2017/07/29/accepted PY - 2017/8/5/pubmed PY - 2018/5/24/medline PY - 2017/8/5/entrez KW - Apoptosis KW - Bone resorption KW - Osteoclast KW - Reactive oxygen species SP - 191 EP - 199 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 112 N2 - 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. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/28774817/Euphorbia_factor_L1_inhibits_osteoclastogenesis_by_regulating_cellular_redox_status_and_induces_Fas_mediated_apoptosis_in_osteoclast_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(17)30712-8 DB - PRIME DP - Unbound Medicine ER -