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Background
Lithium chloride (LiCl) is commonly used in the clinic for the treatment of bipolar and other mental disorders. LiCl is an inhibitor of GSK-3β, and has been reported to modulate the balance of adipogenesis and osteogenesis. But, whether LiCl impacts bone formation and homeostasis in senile osteoporosis is still unclear.
Methods
Analysis of tibia in 2, 5, 7 and 10 months old C57BL/6 male mice were performed by MicroCT (μCT). 7 months old wild-type mice were treated with LiCl orally 0, 100 or 200 mg/kg for 3 months and then tested by μCT. The levels of osteogenesis marker genes and Wnt signaling target genes in bone marrow stromal cells (BMSCs) were detected by reverse transcription quantitative polymerase chain reaction and immunostaining. BMSCs were induced osteoblast differentiation and tested by Alizarin red S staining.
Results
μCT analyses of C57BL/6 mice showed that bone mineral density (BMD) and trabecular thickness (Tb.Th) increased until the bone mass peaked (5 months) and then began to fall subsequently. LiCl dramatically enhanced bone mass in the senile osteoporotic conditions, represented by increased ratio of bone volume to tissue volume (BV/TV), and decreased in trabeculae separation (Tb.Sp). Moreover, LiCl significantly increased both canonical osteoblastogenesis and Wnt signaling activity without affecting hormones.
Conclusion
This study uncovered the role of LiCl in canonical Wnt signaling and bone formation and have provided the evidence that LiCl may potentially repress senile osteoporosis.
Keywords
Lithium chloride, Osteogenesis, Senile osteoporosis, Wnt signaling, Bone marrow-derived mesenchymal stem cells
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A new preprint design is coming!
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 03 Jan, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Orthopedics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Lithium chloride (LiCl) is commonly used in the clinic for the treatment of bipolar and other mental disorders. LiCl is an inhibitor of GSK-3β, and has been reported to modulate the balance of adipogenesis and osteogenesis. But, whether LiCl impacts bone formation and homeostasis in senile osteoporosis is still unclear.
Methods
Analysis of tibia in 2, 5, 7 and 10 months old C57BL/6 male mice were performed by MicroCT (μCT). 7 months old wild-type mice were treated with LiCl orally 0, 100 or 200 mg/kg for 3 months and then tested by μCT. The levels of osteogenesis marker genes and Wnt signaling target genes in bone marrow stromal cells (BMSCs) were detected by reverse transcription quantitative polymerase chain reaction and immunostaining. BMSCs were induced osteoblast differentiation and tested by Alizarin red S staining.
Results
μCT analyses of C57BL/6 mice showed that bone mineral density (BMD) and trabecular thickness (Tb.Th) increased until the bone mass peaked (5 months) and then began to fall subsequently. LiCl dramatically enhanced bone mass in the senile osteoporotic conditions, represented by increased ratio of bone volume to tissue volume (BV/TV), and decreased in trabeculae separation (Tb.Sp). Moreover, LiCl significantly increased both canonical osteoblastogenesis and Wnt signaling activity without affecting hormones.
Conclusion
This study uncovered the role of LiCl in canonical Wnt signaling and bone formation and have provided the evidence that LiCl may potentially repress senile osteoporosis.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
This is a list of supplementary files associated with this preprint. Click to download.
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