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.

中文翻译：

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N-[2-(4-benzoyl-1-piperazinyl)phenyl]-2-(4-chlorophenoxy) 乙酰胺是一种新型的小鼠吸收性骨丢失抑制剂

骨形成和骨吸收之间的动态平衡对于骨量的保持至关重要。破骨细胞（一种降解骨基质的独特细胞）的异常激活可能导致许多骨骼疾病，例如骨质疏松症。骨质疏松症是一种骨代谢疾病，当极端破骨细胞介导的骨吸收超过成骨细胞相关的骨合成时就会发生。因此，鉴定可以调节破骨细胞活性和预防骨质流失引起的骨病的药物具有重要意义。在本研究中，我们发现N-[2-(4-benzoyl-1-piperazinyl)phenyl]-2-(4-chlorophenoxy) 乙酰胺 (PPOAC-Bz) 对破骨细胞生成有很强的抑制作用。PPOAC-Bz 改变了几种破骨细胞特异性标记基因的 mRNA 表达并阻断成熟破骨细胞的形成，抑制 F-肌动蛋白带的形成和体外骨吸收活性。此外，PPOAC-Bz 在体内防止 OVX 诱导的骨质流失。这些发现突出了 PPOAC-Bz 作为治疗溶骨性疾病的前瞻性药物的潜力。