The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China; Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Guangzhou University of Chinese Medicine, Guangzhou, 510405, China; Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
J Ethnopharmacol. 2021 Aug 10;276:114195. doi: 10.1016/j.jep.2021.114195. Epub 2021 May 8.
Plastrum testudinis (PT) is a kind of single traditional Chinese medicine that can tonify kidney and strengthen bone. Plastrum testudinis extract (PTE) has been approved to promote the osteogenic differentiation of bone marrow-derived mesenchymal stem cells in vitro. However, the mechanism by which PTE reduces osteoclast differentiation has not yet been reported.
To explore the potential of PTE as a therapeutic treatment for bone loss caused by senile osteoporosis (SOP).
We evaluated whether PTE could inhibit RANKL-induced osteoclast differentiation both in vitro and in vivo, and investigated PTE-induced phenotypes of human peripheral blood monocytes.
We found that PTE inhibited osteoclast differentiation and bone resorption in vitro in a concentration-dependent manner and that PTE treatment is most effective during the early stages of osteoclastogenesis. Moreover, we found that PTE could block the NF-κB signaling pathway in vitro, leading to the down-regulation of osteoclast-specific genes including C-FOS and NFATC1. The results from our in vivo mouse study suggest that PTE treatment suppresses osteoclast formation and mitigates bone loss caused by SOP. Notably, we also found that PTE inhibited RANKL-induced osteoclast differentiation in human peripheral blood monocytes.
Our results suggest that PTE treatment suppresses osteoclastogenesis and ameliorates bone loss caused by SOP by selectively blocking the nuclear translocation of NF-κB/p50.
药 理 学 意 义:龟板是一种单味中药,具有补肾壮骨的功效。龟板提取物(PTE)已被批准在体外促进骨髓间充质干细胞的成骨分化。然而,PTE 抑制破骨细胞分化的机制尚未报道。
研 究 目 的:探讨 PTE 作为治疗老年性骨质疏松症(SOP)所致骨丢失的潜在治疗方法。
材 料 和 方 法:我们评估了 PTE 是否可以在体外和体内抑制 RANKL 诱导的破骨细胞分化,并研究了 PTE 诱导人外周血单核细胞的表型。
结 果:我们发现 PTE 以浓度依赖的方式抑制体外破骨细胞分化和骨吸收,并且 PTE 治疗在破骨细胞发生的早期阶段最有效。此外,我们发现 PTE 可以阻断体外 NF-κB 信号通路,导致破骨细胞特异性基因(包括 C-FOS 和 NFATC1)下调。我们的体内小鼠研究结果表明,PTE 治疗可抑制破骨细胞形成并减轻 SOP 引起的骨丢失。值得注意的是,我们还发现 PTE 抑制了 RANKL 诱导的人外周血单核细胞中的破骨细胞分化。
结 论:我们的结果表明,PTE 治疗通过选择性阻断 NF-κB/p50 的核易位来抑制破骨细胞发生,从而改善 SOP 引起的骨丢失。