Orthopedic Department, Taizhou Hospital Affiliated to Wenzhou Medical University, Linhai 317000, China; Bone development and metabolism research center of Taizhou Hospital, Linhai 317000, China.
Enze Medical Research Center, Taizhou Hospital Affiliated to Wenzhou Medical University, Linhai 317000, China; Bone development and metabolism research center of Taizhou Hospital, Linhai 317000, China.
Eur J Pharmacol. 2019 Apr 5;848:96-104. doi: 10.1016/j.ejphar.2019.01.021. Epub 2019 Jan 23.
[4-(acetylamino)-N-(2-amino-phenyl) benzamide] (CI-994) is a histone deacetylase 1-3 specific inhibitor that has been shown to indirectly increase the production of Dickkopf-1, which is an inhibitor of osteoclastic development. However, whether CI-994 has an influence on receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis is still unclear; in our study, this mechanism was investigated. In an in vitro study, using a tartrate-resistant acid phosphatase (TRAP) stain, an F-actin ring, bone absorption test, quantitative PCR and Western blotting, the role of CI-994 in osteoclastogenesis and the expression of related genes and proteins were investigated. In an in vivo study, the effect of CI-994 on osteolysis was evaluated using a titanium particle-induced murine calvarial osteolysis model. Our results indicated that CI-994 inhibited osteoclast differentiation and the function of bone resorption without cytotoxic effects. Moreover, CI-994 inhibited the expression of osteoclast-related genes, including ACP5, CTSK, NFATc1, c-Fos, DC-STAMP and V-ATPase-d2. Furthermore, CI-994 suppressed the phosphorylation of IκBα and p65 and the expression of downstream c-Fos and NFATc1. Consistent with the in vitro results described above, our in vivo experiment indicated that CI-994 inhibited Ti-induced osteolysis. In conclusion, CI-994 inhibited osteoclastogenesis by suppressing NF-κB and the downstream c-Fos/NFATc1 signaling pathway. Thus, this study showed the possibility of using CI-994 for the treatment of exorbitant osteoclastic bone resorption.
[4-(乙酰氨基)-N-(2-氨基苯基)苯甲酰胺](CI-994)是一种组蛋白去乙酰化酶 1-3 特异性抑制剂,已被证明可间接增加 Dickkopf-1 的产生,Dickkopf-1 是破骨细胞发育的抑制剂。然而,CI-994 是否对核因子-κB 受体激活剂配体(RANKL)诱导的破骨细胞生成有影响尚不清楚;在本研究中,我们对此机制进行了研究。在体外研究中,我们使用抗酒石酸酸性磷酸酶(TRAP)染色、F-肌动蛋白环、骨吸收试验、定量 PCR 和 Western blot 研究了 CI-994 在破骨细胞生成中的作用以及相关基因和蛋白的表达。在体内研究中,我们使用钛颗粒诱导的小鼠颅骨骨溶解模型评估了 CI-994 对骨溶解的作用。结果表明,CI-994 抑制破骨细胞分化和骨吸收功能,而无细胞毒性作用。此外,CI-994 抑制了破骨细胞相关基因的表达,包括 ACP5、CTSK、NFATc1、c-Fos、DC-STAMP 和 V-ATPase-d2。此外,CI-994 抑制了 IκBα 和 p65 的磷酸化以及下游 c-Fos 和 NFATc1 的表达。与上述体外结果一致,我们的体内实验表明 CI-994 抑制了 Ti 诱导的骨溶解。总之,CI-994 通过抑制 NF-κB 及其下游 c-Fos/NFATc1 信号通路抑制破骨细胞生成。因此,本研究表明了使用 CI-994 治疗过度破骨细胞骨吸收的可能性。