Beta-Ecdysone Protects Mouse Osteoblasts from Glucocorticoid-Induced Apoptosis In Vitro
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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The effect of glucocorticoid on osteoclast viability was reverted by 20E.
“This was reverted by 20E in agreement with the in vivo bone protective and GC side effect neutralizing potential of the phytoecdysteroid.”
From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [37]
In vitro treatment with glucocorticoid decreased osteoclast viability by decreasing differentiation markers and increasing a wide range of apoptotic factors.
“In vitro treatment with GC decreased osteoclast viability by decreasing differentiation markers and increasing a wide range of apoptotic factors [37].”
From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [37]
PEs isolated from Vitex doniana act as an antidepressant.
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From Phytoecdysteroids: Distribution, Structural Diversity, Biosynthesis, Activity, and Crosstalk with Phytohormones (2022) · cites this paper as [163]
ECs reduce adverse effects of stress by inducing release of glucocorticoids in mice.
“ECs reduce the adverse effects of stress by inducing the release of glucocorticoids in mice [163].”
From Phytoecdysteroids: Distribution, Structural Diversity, Biosynthesis, Activity, and Crosstalk with Phytohormones (2022) · cites this paper as [163]
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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
- Publisher
- Georg Thieme Verlag KG
- Published
- 2017-04-07
- Volume
- 83
- Issue
- 11
- Pages
- 888-894
- ISSN
- 0032-0943 (ISSN-L)
- 1439-0221
- OpenAlex
- W2604817892
- Semantic Scholar
- a848bc26c071fb4835a336d9164fb18373f07237
- 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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