Plumbagin, a Biomolecule with (Anti)Osteoclastic Properties

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 apoptos...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-03, Vol.22 (5), p.2779
Main Authors: Sultanli, Sevinj, Ghumnani, Soni, Ashma, Richa, Kubatzky, Katharina F
Format: Article
Language:English
Subjects:
Animals
Bone Resorption - drug therapy
Bone Resorption - metabolism
Bone Resorption - pathology
Macrophage Colony-Stimulating Factor - metabolism
Mice
mTOR
Naphthoquinones - pharmacology
NFATC Transcription Factors - metabolism
osteoclast
Osteoclasts - metabolism
Osteoclasts - pathology
phytotherapy
plumbagin
RANK Ligand - metabolism
RAW 264.7 Cells
ROS
TOR Serine-Threonine Kinases - metabolism
translation
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22052779