Chen Z(1), Cho E(2), Ding M(1), Seong J(2), Che X(3), Lee S(4), Park BJ(2), Choi JY(3), Lee TH(1)(2). Author information:
(1)Department of Molecular Medicine, Chonnam National University Graduate
School, Gwangju, Korea.
(2)Department of Oral Biochemistry, Dental Science Research Institute, Korea
Mouse Phenotyping Center, School of Dentistry, Chonnam National University,
(3)Department of Biochemistry and Cell Biology, Cell and Matrix Research
Institute, Korea Mouse Phenotyping Center, KNU Convergence Educational Program
of Biomedical Sciences for Creative Future Talents, School of Medicine,
Kyungpook National University, Daegu, Korea.
(4)Department of Chemistry, Chonnam National University, Gwangju, Korea.
The dynamic balance between bone formation and bone resorption is vital for the retention of bone mass. The abnormal activation of osteoclasts, unique cells that degrade the bone matrix, may result in many bone diseases such as osteoporosis. Osteoporosis, a bone metabolism disease, occurs when extreme osteoclast-mediated bone resorption outstrips osteoblast-related bone synthesis. Therefore, it is of great interest to identify agents that can regulate the activity of osteoclasts and prevent bone loss-induced bone diseases. In this study, we found that N-[2-(4-benzoyl-1-piperazinyl)phenyl]-2-(4-chlorophenoxy) acetamide (PPOAC-Bz) exerted a strong inhibitory effect on osteoclastogenesis. PPOAC-Bz altered the mRNA expressions of several osteoclast-specific marker genes and blocked the formation of mature osteoclasts, suppressing F-actin belt formation and bone resorption activity in vitro. In addition, PPOAC-Bz prevented OVX-induced bone loss in vivo. These findings highlighted the potential of PPOAC-Bz as a prospective drug for the treatment of osteolytic disorders.
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