ArticleAging2022
Polydatin administration attenuates the severe sublesional bone loss in mice with chronic spinal cord injury.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Unraveling the Skeletal Growth-Promoting Mechanism of the SeahorseCurrent issues in molecular biology · 2026Article
- Polydatin for treating spinal cord injury: Multiple mechanisms and challenges.Journal of pharmaceutical analysis · 2026Review
- Polydatin Reverses Diabetes-Induced Apoptosis of Pancreatic β-Cells by Inhibiting the TNF/TNF-R1/Caspase-3 Signaling Axis.Journal of diabetes research · 2026Article
- Polydatin attenuated neuropathic pain and motor dysfunction following spinal cord injury in rats by employing its anti-inflammatory and antioxidant effects.Frontiers in pharmacology · 2024Article
- Pro-Osteogenic and Anti-Inflammatory Synergistic Effect of Orthosilicic Acid, Vitamin K2, Curcumin, Polydatin and Quercetin Combination in Young and Senescent Bone Marrow-Derived Mesenchymal Stromal Cells.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSpinal cord injury (SCI) is often accompanied by rapid and extensive bone mineral loss below the lesion level, and there is currently no gold standard for treatment. Evidence suggests that polydatin (PLD) may help promote osteogenic differentiation and exhibit anti-osteoporotic activity. However, whether PLD could reverse substantial bone loss in SCI patients, especially those with protracted injury, and the underlying regulatory mechanism have not been investigated. STUDY
designMale C57BL/6J mice were subjected to either contusion SCI or laminectomy at the T
resultsChronic SCI led to a rapid and significant decrease in bone mineral density (BMD) of the distal femur and proximal tibia, resulting in structural deterioration of the bone tissues. Treatment with PLD largely restored BMD and bone structure. In addition, static histo-morphometric analysis revealed that PLD enhanced bone formation and inhibited bone resorption
conclusionsPLD protected mice with chronic SCI against sublesional bone loss by modulating genes involved the differentiation and activity of osteoclasts and osteoblasts, abating oxidative stress and MMP activity, and restoring the Wnt/β-catenin signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.