ArticleFrontiers in pharmacology2022
Epimedin C Alleviates Glucocorticoid-Induced Suppression of Osteogenic Differentiation by Modulating PI3K/AKT/RUNX2 Signaling Pathway.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Adipose-derived stem cell exosomes mitigate ferroptosis and enhance osteogenesis via miR-215-5p-mediated ubiquitin-specific protease 1 suppression.Endocrine journal · 2026Article
- Exploring the effects and mechanisms of Chinese yam in treating osteoporosis using network pharmacology analysis and biological validation.Scientific reports · 2026Article
- A comprehensive narrative review ofJournal of pharmaceutical analysis · 2026Review
- Therapeutic potential of natural products from Traditional Chinese Medicine in the treatment of osteoporosis.Frontiers in pharmacology · 2026Review
- The 3D printed biphasic scaffolds incorporating epimedin C promotes osteochondral regeneration in osteoarthritis rats.Regenerative biomaterials · 2026Article
- Rapid osteointegration with a strontium-containing hydroxyapatite coating on tantalum by activating Itga6-PI3K/AKT signaling pathway.Materials today. Bio · 2025Article
- Histone H3K18 lactylation-dependent epigenetic activation of RUNX2 orchestrates PI3K/AKT oncogenic signaling in laryngeal squamous cell carcinoma.Journal of molecular histology · 2025Article
- An engineered M2 macrophage-derived exosomes-loaded electrospun biomimetic periosteum promotes cell recruitment, immunoregulation, and angiogenesis in bone regeneration.Bioactive materials · 2025Article
- The active metabolite of Epimedii Folium promotes hippocampal neurogenesis in APP/PS1 mice by alleviating mitochondrial dysfunction.Frontiers in pharmacology · 2025Article
- Aligned nanofibers in biomimetic periosteal extracellular matrix/poly(ε-caprolactone) membranes enhance bone regeneration via the ITGB1/PI3K/AKT pathway.Regenerative biomaterials · 2025Article
- Epimedin C alleviated osteoarthritis development by regulating chondrocyte Nrf2-mediated NLRP3 inflammasome axis.Heliyon · 2024Article
- Injectable, oxygen-releasing, thermosensitive hydrogel promotes vascularized bone formation with prolonged oxygen delivery and improved osteoinductivity.Materials today. Bio · 2024Article
- Functions of Epimedin C in a zebrafish model of glucocorticoid-induced osteoporosis.Journal of cellular and molecular medicine · 2024Article
- Mesenchymal stem cells under epigenetic control - the role of epigenetic machinery in fate decision and functional properties.Cell death & disease · 2023Review
- Advancements in the Biotransformation and Biosynthesis of the Primary Active Flavonoids Derived fromMolecules (Basel, Switzerland) · 2023Review
- Kidney tonifying traditional Chinese medicine: Potential implications for the prevention and treatment of osteoporosis.Frontiers in pharmacology · 2022Review
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9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Secondary osteoporosis is triggered mostly by glucocorticoid (GC) therapy. Dexamethasone (DEX) was reported to inhibit osteogenic differentiation in zebrafish larvae and MC3T3-E1 cells in prior research. In this research, we primarily examined the protective impacts of epimedin C on the osteogenic inhibition impact of MC3T3-E1 cells and zebrafish larvae mediated by DEX. The findings illustrated no apparent toxicity for MC3T3-E1 cells after administering epimedin C at increasing dosages from 1 to 60 μM and no remarkable proliferation in MC3T3-E1 cells treated using DEX. In MC3T3-E1 cells that had been treated using DEX, we discovered that epimedin C enhanced alkaline phosphatase activities and mineralization. Epimedin C could substantially enhance the protein expression of osterix (OSX), Runt-related transcription factor 2 (RUNX2), and alkaline phosphatase (ALPL) in MC3T3-E1 cells subjected to DEX treatment. Additionally, epimedin C stimulated PI3K and AKT signaling pathways in MC3T3-E1 cells that had been treated using DEX. Furthermore, in a zebrafish larvae model, epimedin C was shown to enhance bone mineralization in DEX-mediated bone impairment. We also found that epimedin C enhanced ALPL activity and mineralization in MC3T3-E1 cells treated using DEX, which may be reversed by PI3K inhibitor (LY294002). LY294002 can also reverse the protective impact of epimedin C on DEX-mediated bone impairment in zebrafish larval. These findings suggested that epimedin C alleviated the suppressive impact of DEX on the osteogenesis of zebrafish larval and MC3T3-E1 cells via triggering the PI3K and AKT signaling pathways. Epimedin C has significant potential in the development of innovative drugs for the treatment of glucocorticoid-mediated osteoporosis.
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