ArticleCellular and molecular neurobiology2018
Inhibition of Autophagy is Involved in the Protective Effects of Ginsenoside Rb1 on Spinal Cord Injury.
Article in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Ginseng alleviates fatigue by inhibiting autophagy via activation of the PI3K/AKT/mTOR signaling pathway.Molecular biology reports · 2026Article
- A Review of the Potential Use of Antioxidants in Spinal Cord Injuries.Antioxidants (Basel, Switzerland) · 2025Review
- Vimentin Inhibits Neuronal Apoptosis After Spinal Cord Injury by Enhancing Autophagy.CNS neuroscience & therapeutics · 2025Article
- Progress of Ginsenoside Rb1 in neurological disorders.Frontiers in pharmacology · 2024Review
- Tibolone Improves Locomotor Function in a Rat Model of Spinal Cord Injury by Modulating Apoptosis and Autophagy.International journal of molecular sciences · 2023Article
- The Temporal and Spatial Changes of Autophagy and PI3K Isoforms in Different Neural Cells After Hypoxia/Reoxygenation Injury.Molecular neurobiology · 2023Article
- Ginsenoside Rb1 attenuates methamphetamine (METH)-induced neurotoxicity through the NR2B/ERK/CREB/BDNF signalingsJournal of ginseng research · 2022Article
- Recent progress (2015-2020) in the investigation of the pharmacological effects and mechanisms of ginsenoside RbJournal of ginseng research · 2022Review
- Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases.Frontiers in pharmacology · 2022Review
- Ginseng extract and ginsenosides improve neurological function and promote antioxidant effects in rats with spinal cord injury: A meta-analysis and systematic review.Journal of ginseng research · 2022Review
- Insulin-like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway.Experimental and therapeutic medicine · 2021Article
- AAV2-mediated and hypoxia response element-directed expression of bFGF in neural stem cells showed therapeutic effects on spinal cord injury in rats.Cell death & disease · 2021Article
- Biological Functions and Therapeutic Potential of Autophagy in Spinal Cord Injury.Frontiers in cell and developmental biology · 2021Review
- Paving the Road Toward Exploiting the Therapeutic Effects of Ginsenosides: An Emphasis on Autophagy and Endoplasmic Reticulum Stress.Advances in experimental medicine and biology · 2021Article
- Modulation of autophagy for neuroprotection and functional recovery in traumatic spinal cord injury.Neural regeneration research · 2020Review
- Therapeutic effect of regulating autophagy in spinal cord injury: a network meta-analysis of direct and indirect comparisons.Neural regeneration research · 2020Article
- AMP-activated protein kinase-dependent induction of autophagy by erythropoietin protects against spinal cord injury in rats.CNS neuroscience & therapeutics · 2018Article
- Targeting Cellular Stress Mechanisms and Metabolic Homeostasis by Chinese Herbal Drugs for Neuroprotection.Molecules (Basel, Switzerland) · 2018Review
- Cell Specific Changes of Autophagy in a Mouse Model of Contusive Spinal Cord Injury.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Spinal cord injury (SCI) is a devastating neurological disorder. Autophagy is induced and plays a crucial role in SCI. Ginsenoside Rb1 (Rb1), one of the major active components extracted from Panax Ginseng CA Meyer, has exhibited neuroprotective effects in various neurodegenerative diseases. However, it remains unknown whether autophagy is involved in the neuroprotection of Rb1 on SCI. In this study, we examined the regulation of autophagy following Rb1 treatment and its involvement in the Rb1-induced neuroprotection in SCI and in vitro injury model. Firstly, we found that Rb1 treatment decreased the loss of motor neurons and promoted function recovery in the SCI model. Furthermore, we found that Rb1 treatment inhibited autophagy in neurons, and suppressed neuronal apoptosis and autophagic cell death in the SCI model. Finally, in the in vitro injury model, Rb1 treatment increased the viability of PC12 cells and suppressed apoptosis by inhibiting excessive autophagy, whereas stimulation of autophagy by rapamycin abolished the anti-apoptosis effect of Rb1. Taken together, these findings suggest that the inhibition of autophagy is involved in the neuroprotective effects of Rb1 on SCI.
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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.