Zentrum für Infektiologie, Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany.
Department of Zoology, Savitribai Phule Pune University, Pune 411007, India.
Int J Mol Sci. 2021 Mar 9;22(5):2779. doi: 10.3390/ijms22052779.
Plumbagin is a plant-derived naphthoquinone that is widely used in traditional Asian medicine due to its anti-inflammatory and anti-microbial properties. Additionally, plumbagin is cytotoxic for cancer cells due to its ability to trigger reactive oxygen species (ROS) formation and subsequent apoptosis. Since it was reported that plumbagin may inhibit the differentiation of bone resorbing osteoclasts in cancer-related models, we wanted to elucidate whether plumbagin interferes with cytokine-induced osteoclastogenesis. Using C57BL/6 mice, we unexpectedly found that plumbagin treatment enhanced osteoclast formation and that this effect was most pronounced when cells were pre-treated for 24 h with plumbagin before subsequent M-CSF/RANKL stimulation. Plumbagin caused a fast induction of NFATc1 signalling and mTOR-dependent activation of p70S6 kinase which resulted in the initiation of protein translation. In line with this finding, we observed an increase in RANK surface expression after Plumbagin stimulation that enhanced the responsiveness for subsequent RANKL treatment. However, in Balb/c mice and Balb/c-derived RAW264.7 macrophages, these findings could not be corroborated and osteoclastogenesis was inhibited. Our results suggest that the effects of plumbagin depend on the model system used and can therefore either trigger or inhibit osteoclast formation.
白花丹醌是一种植物来源的萘醌,由于其具有抗炎和抗菌特性,因此在传统的亚洲医学中被广泛使用。此外,白花丹醌能够触发活性氧 (ROS) 的形成,并随后诱导细胞凋亡,因此对癌细胞具有细胞毒性。由于有报道称白花丹醌可能会抑制癌症相关模型中破骨细胞的分化,因此我们想要阐明白花丹醌是否会干扰细胞因子诱导的破骨细胞生成。我们使用 C57BL/6 小鼠,出乎意料地发现白花丹醌处理会增强破骨细胞的形成,并且在随后的 M-CSF/RANKL 刺激之前,细胞用白花丹醌预处理 24 小时,这种作用最为明显。白花丹醌会快速诱导 NFATc1 信号通路,并导致 mTOR 依赖性激活 p70S6 激酶,从而启动蛋白质翻译。与这一发现一致,我们观察到在白花丹醌刺激后 RANK 表面表达增加,从而增强了对随后的 RANKL 处理的反应性。但是,在 Balb/c 小鼠和 Balb/c 衍生的 RAW264.7 巨噬细胞中,无法证实这些发现,并且破骨细胞生成受到抑制。我们的结果表明,白花丹醌的作用取决于所使用的模型系统,因此可以触发或抑制破骨细胞的形成。