ArticleStem cell research & therapy2022
Aucubin promotes bone-fracture healing via the dual effects of anti-oxidative damage and enhancing osteoblastogenesis of hBM-MSCs.
Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 25 citations in OpenAlex.
- Rapid maxillary expansion related sutural and dentoalveolar changes provoke early-term oxidative stress.BMC oral health · 2026Trial
- Iridoids as Multi-target Neuroprotective Agents for Ischemic Stroke: Mechanisms and Therapeutic Potential.Mini reviews in medicinal chemistry · 2026Review
- Salvianolic acid B ameliorates vascular calcification in rats with chronic kidney disease combined with arteriovenous fistula by inhibiting BMP2/Smads signaling.Renal failure · 2025Article
- Oxidative Stress and Biomarkers in Craniofacial Fractures Healing: From Lipid Peroxidation to Antioxidant Therapies.Antioxidants (Basel, Switzerland) · 2025Review
- Traditional medicine in a modern light: a scoping review on the osteoprotective potential ofFrontiers in pharmacology · 2025Review
- NQO1 promotes osteogenesis and suppresses angiogenesis in DPSCs via MAPK pathway modulation.Stem cell research & therapy · 2024Article
- Extraction and Purification of Aucubin fromACS omega · 2024Article
- The role of current herbal extracts in bone regeneration through dental implants:Archives of medical science : AMS · 2023Article
- Aloe polysaccharide promotes osteogenesis potential of adipose-derived stromal cells via BMP-2/Smads and prevents ovariectomized-induced osteoporosis.Molecular biology reports · 2022Article
- Primary cilia: The central role in the electromagnetic field induced bone healing.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
backgroundAucubin (AU), an iridoid glucoside isolated from many traditional herbal medicines, has anti-osteoporosis and anti-apoptosis bioactivities. However, the effect of AU on the treatment of bone-fracture remains unknown. In the present study, the aims were to investigate the roles and mechanisms of AU not only on osteoblastogenesis of human bone marrow-derived mesenchymal stromal cells (hBM-MSCs) and anti-oxidative stress injury in vitro, but also on bone-fracture regeneration by a rat tibial fracture model in vivo.
methodsCCK-8 assay was used to assess the effect of AU on the viability and proliferation of hBM-MSCs. The expression of specific genes and proteins on osteogenesis, apoptosis and signaling pathways was measured by qRT-PCR, western blotting and immunofluorescence analysis. ALP staining and quantitative analysis were performed to evaluate ALP activity. ARS and quantitative analysis were performed to evaluate calcium deposition. DCFH-DA staining was used to assess the level of reactive oxygen species (ROS). A rat tibial fracture model was established to validate the therapeutic effect of AU in vivo. Micro-CT with quantitative analysis and histological evaluation were used to assess the therapeutic effect of AU locally injection at the fracture site.
resultsOur results revealed that AU did not affect the viability and proliferation of hBM-MSCs. Compared with control group, western blotting, PCR, ALP activity and calcium deposition proved that AU-treated groups promoted osteogenesis of hBM-MSCs. The ratio of phospho-Smad1/5/9 to total Smad also significantly increased after treatment of AU. AU-induced expression of BMP2 signaling target genes BMP2 and p-Smad1/5/9 as well as of osteogenic markers COL1A1 and RUNX2 was downregulated after treating with noggin and LDN193189. Furthermore, AU promoted the translocation of Nrf2 from cytoplasm to nucleus and the expression level of HO1 and NQO1 after oxidative damage. In a rat tibial fracture model, local injection of AU promoted bone regeneration.
conclusionsOur study demonstrates the dual effects of AU in not only promoting bone-fracture healing by regulating osteogenesis of hBM-MSCs partly via canonical BMP2/Smads signaling pathway but also suppressing oxidative stress damage partly via Nrf2/HO1 signaling pathway.
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