Cited by 22Bone Metabolism and DiseasesBone health and osteoporosis researchEstrogen and related hormone effects

Beta-Ecdysone Protects Mouse Osteoblasts from Glucocorticoid-Induced Apoptosis In Vitro

Dai, Wei-Wei, Wang, Li-Bo, Jin, Guo-Qin, Wu, Hong-Jin, Zhang, Jie, Wang, Cheng-Long, Wei, Yuan-Ji, Lee, Joon-Ho +2 more·2017·Planta Medica

Abstract

Glucocorticoid-induced osteoporosis is a common form of secondary osteoporosis. Glucocorticoids affect both bone formation and resorption, and prolonged glucocorticoid exposure can suppress osteoblast activities. beta-Ecdysone, found in many plants, is involved in protein synthesis, carbohydrate and lipid metabolism, and immunologic modulation. Here, we evaluated the effects of beta-ecdysone on osteoblast viability by assessing apoptosis following treatment with excess glucocorticoids. Mouse bone marrow stromal cells were induced to differentiate and grow into osteoblasts, and then treated with 10 µM glucocorticoid and 10, 1, or 0.1 µM beta-ecdysone. The expression levels of osteoblast growth and differentiation factors (runt-related transcription factor 2, osteogenic protein-1, and alkaline phosphatase), apoptosis-related genes (transformation-related protein 53, ataxia telangiectasia mutated protein, caspase-3, and caspase-8), and Akt1 and phospho-Akt (Thr308) were then assessed via alkaline phosphatase staining, acridine orange-propidium iodide staining, annexin V/PI apoptosis assay, real-time RT-PCR, and Western blot analyses. Notably, treatment with 10 µM glucocorticoid resulted in reduced osteoblast viability and the specific activity of alkaline phosphatase as well as reduced runt-related transcription factor 2, osteogenic protein-1, and alkaline phosphatase mRNA expression in vitro, indicating that glucocorticoid inhibited osteogenic differentiation. Moreover, glucocorticoid treatment yielded increased transformation-related protein 53, ataxia telangiectasia mutated protein, caspase-3, and caspase-8 expression and decreased Akt1 and phospho-Akt levels, indicating glucocorticoid-induced apoptosis. Meanwhile, beta-ecdysone inhibited glucocorticoid function, preserving the expression of Akt1 and phospho-Akt and reducing the expression of transformation-related protein 53, ataxia telangiectasia mutated protein, caspase-3, and caspase-8. Thus, beta-ecdysone prevented glucocorticoid-induced osteoblast apoptosis in vitro. These data highlight the potential for beta-ecdysone as a treatment for preventing the effects of glucocorticoid on bone growth.

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Crossref · 10.1055/s-0043-107808

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Authors
Dai, W.-W., Wang, L.-B., Jin, G.-Q., Wu, H.-J., Zhang, J., Wang, C.-L., Wei, Y.-J., Lee, J.-H., Lay, Y.-A., & Yao, W.
Affiliations
  • Shanghai University of Traditional Chinese Medicine (CN)
  • Department of Biochemistry, Integrative Medicine Discipline, Shanghai University of Traditional Chinese Medicine, Shanghai, China
  • University of California Davis Medical Center (US)
Venue
Planta Medica
Published
2017-04-07
Volume
83
Issue
11
Pages
888-894
ISSN
  • 0032-0943 (ISSN-L)
  • 1439-0221
OpenAlex
W2604817892
Cited by
22
References
43
Citations by year
2026: 1 · 2025: 5 · 2024: 1 · 2023: 1 · 2022: 6 · 2021: 3 · 2020: 2 · 2019: 1 · 2017: 2
FWCI
0.56
Type
journal article
Language
en
Open access
closed
Locations
  • Planta Medica (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Keywords
20-hydroxyecdysone, glucocorticoid-induced osteoporosis, glucocorticoid-induced apoptosis, osteoblasts, osteogenic differentiation, Akt signaling, caspase-3, caspase-8, p53, ATM, alkaline phosphatase, Runx2, osteogenic protein-1, mesenchymal stem cells, secondary osteoporosis
MeSH terms
Animals, Cell Survival, Cells, Cultured, Ecdysterone, Glucocorticoids, Male, Mice, Inbred BALB C, Osteoblasts, Plants, Medicinal, Mifepristone, Apoptosis, Mice

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