ArticleJOR spine2024
Silibinin promotes healing in spinal cord injury through anti-ferroptotic mechanisms.
Article in JOR spine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- MicroRNA-Ferroptosis-Spinal Cord Injury: A Complex Interplay in Neurodegeneration and Repair.International journal of molecular sciences · 2026Review
- A dual-pronged strategy: multi-bioactive nanoplatform synergizes ROS antidote and iron stabilization to protect against liver ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Article
- Interference with HMGB1 Inhibits Neuronal Ferroptosis Following Spinal Cord Injury through Targeting ACSL4.Neurochemical research · 2026Article
- Low-Dose Lipopolysaccharide Alleviates Neuronal Apoptosis and Oxidative Stress in Rats with Spinal Cord Injury by Inducing Nrf2 m6A Methylation Modification via Suppressing ALKBH5.Neurochemical research · 2025Article
- Natural products protect against spinal cord injury by inhibiting ferroptosis: a literature review.Frontiers in pharmacology · 2025Review
- Intrathecal silymarin administration improves recovery after compression spinal cord injury: evidence for neuroprotection, antioxidant, and anti-inflammatory action.Frontiers in pharmacology · 2025Article
- Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis.Cell death discovery · 2024Review
- Silibinin promotes healing in spinal cord injury through anti-ferroptotic mechanisms.JOR spine · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Study Design: Pre-clinical animal experiment. Objective: In this study, we investigated therapeutic effects of silibinin in a spinal cord injury (SCI) model. In SCI, loss of cells due to secondary damage mechanisms exceeds that caused by primary damage. Ferroptosis, which is iron-dependent non-apoptotic cell death, is shown to be influential in the pathogenesis of SCI. Methods: The study was conducted as an in vivo experiment using a total of 78 adult male/female Sprague Dawley rats. Groups were as follows: Sham, SCI, deferoxamine (DFO) treatment, and silibinin treatment. There were subgroups with follow-up periods of 24 h, 72 h, and 6 weeks in all groups. Malondialdehyde (MDA), glutathione (GSH), and Fe Results: Silibinin achieved significant suppression in MDA and 4-HNE levels compared to the SCI both in 72-h and 6 weeks group ( Conclusion: Impact of silibinin on iron metabolism and lipid peroxidation, both of which are features of ferroptosis, may contribute to therapeutic activity. Within this context, our findings posit silibinin as a potential therapeutic candidate possessing antiferroptotic properties in SCI model. Therapeutic agents capable of effectively and safely mitigating ferroptotic cell death hold the potential to be critical points of future clinical investigations.
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