ArticleNeural regeneration research2023
Ginsenoside Rb1 improves energy metabolism after spinal cord injury.
Article in Neural regeneration research, 2023. 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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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- A Unified Framework for Spinal Cord Injury Repair: Metabolic-Nutritional Microenvironment Remodeling, Immune Modulation, and Neural Regeneration.Molecular neurobiology · 2026Review
- Natural Products and Neuroregeneration: Rethinking Discovery Beyond Bioavailability Through Pseudo-Natural Product Design.Biomedicines · 2026Review
- Food-Medicine Homologous Qiongyu Gao Attenuates Skin Photoaging by Remodeling Gut Microbiota and Restoring Mitochondrial Energy Metabolism.Foods (Basel, Switzerland) · 2026Article
- Overcoming Barriers to Axonal Regeneration in Spinal Cord Injury: Mechanistic Insights and Therapeutic Frontiers.CNS neuroscience & therapeutics · 2026Review
- Adipose tissue-derived stromal cells enhance glycolytic metabolism in injured nerve cells via the FOXK1-HK2 axis for spinal cord injury repair.Journal of translational medicine · 2026Article
- Ginseng-Derived Carbon Quantum Dots Enhance Systemic Exposure of Bioactive Ginsenosides and Amplify Energy Metabolism in Mice.Pharmaceutics · 2025Article
- Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.Cellular and molecular neurobiology · 2025Review
- The biological functions of ginsenoside and its applications in animal husbandry.Frontiers in veterinary science · 2025Review
- Inhibition of UHRF1 Improves Motor Function in Mice with Spinal Cord Injury.Cellular and molecular neurobiology · 2024Article
- Progress of Ginsenoside Rb1 in neurological disorders.Frontiers in pharmacology · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial damage caused by oxidative stress and energy deficiency induced by focal ischemia and hypoxia are important factors that aggravate diseases. Studies have shown that ginsenoside Rb1 has neurotrophic and neuroprotective effects. However, whether it influences energy metabolism after spinal cord injury remains unclear. In this study, we treated mouse and cell models of spinal cord injury with ginsenoside Rb1. We found that ginsenoside Rb1 remarkably inhibited neuronal oxidative stress, protected mitochondria, promoted neuronal metabolic reprogramming, increased glycolytic activity and ATP production, and promoted the survival of motor neurons in the anterior horn and the recovery of motor function in the hind limb. Because sirtuin 3 regulates glycolysis and oxidative stress, mouse and cell models of spinal cord injury were treated with the sirtuin 3 inhibitor 3-TYP. When Sirt3 expression was suppressed, we found that the therapeutic effects of ginsenoside Rb1 on spinal cord injury were remarkably inhibited. Therefore, ginsenoside Rb1 is considered a potential drug for the treatment of spinal cord injury, and its therapeutic effects are closely related to sirtuin 3.
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