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Aucubin slows the development of osteoporosis by inhibiting osteoclast differentiation via the nuclear factor
Yongfeng Zhang1,2, Xin Liu2, Yangyang Li1
1Department of Orthodontics, School and Hospital of Stomatology, Jilin University, Changchun, China.
Context:
Osteoporosis (OP) is a metabolic disease. We have previously demonstrated that aucubin (AU) has anti-OP effects that are due to its promotion of the formation of osteoblasts.
Objectives:
To investigate the mechanisms of anti-OP effects of AU.
Materials And Methods:
C57BL/6 mice were randomly divided into control group, 30 mg/kg Dex-induced OP group (OP model group, 15 μg/kg oestradiol-treated positive control group, 5 or 45 mg/kg AU-treated group), and 45 mg/kg AU-alone-treated group. The administration lasted for 7 weeks. Subsequently, 1, 2.5 and 5 µM AU were incubated with 50 ng/mL RANKL-induced RAW264.7 cells for 7 days to observe osteoclast differentiation. The effect of AU was evaluated by analysing tissue lesions, biochemical factor and protein expression.
Results:
The LD50 of AU was greater than 45 mg/kg. AU increased the number of trabeculae and reduced the loss of chondrocytes in OP mice. Compared to OP mice, AU-treated mice exhibited decreased serum concentrations of TRAP5b (19.6% to 28.4%), IL-1 (12.2% to 12.6%), IL-6 (12.1%) and ROS (5.9% to 10.7%) and increased serum concentrations of SOD (14.6% to 19.4%) and CAT (17.2% to 27.4%). AU treatment of RANKL-exposed RAW264.7 cells decreased the numbers of multi-nuclear TRAP-positive cells, reversed the over-expression of TRAP5, NFATc1 and CTSK. Furthermore, AU increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins in RANKL-exposed RAW264.7 cells.
Conclusions:
AU slows the development of OP via Nrf2-mediated antioxidant pathways, indicating the potential use of AU in OP therapy and other types of OP research.
Insights
Aucubin (AU) effectively slows osteoporosis development by promoting osteoblast formation and activating Nrf2-mediated antioxidant pathways. This research highlights AU
Area of Science:
- Pharmacology
- Cell Biology
- Biochemistry
Background:
- Osteoporosis (OP) is a significant metabolic bone disease.
- Previous studies indicated aucubin (AU) promotes osteoblast formation, suggesting anti-OP effects.
Purpose of the Study:
- To elucidate the specific mechanisms underlying the anti-osteoporosis effects of aucubin (AU).
Main Methods:
- In vivo studies using C57BL/6 mice with dexamethasone-induced OP, treated with varying AU doses.
- In vitro studies involving RAW264.7 cells treated with AU and RANKL to assess osteoclast differentiation.
- Analysis of tissue lesions, serum biochemical markers, and protein expression.
Main Results:
- Aucubin (AU) treatment increased trabecular bone number and reduced chondrocyte loss in OP mice.
- AU administration decreased serum levels of TRAP5b, IL-1, IL-6, and ROS, while increasing SOD and CAT.
- In vitro, AU inhibited osteoclast differentiation and reversed the overexpression of TRAP5, NFATc1, and CTSK, alongside upregulating Nrf2 and its downstream proteins.
Conclusions:
- Aucubin (AU) mitigates osteoporosis progression through Nrf2-mediated antioxidant pathways.
- These findings support the potential therapeutic application of AU in osteoporosis treatment and research.
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