ArticleNeurochemical research2015
Mitochondrial Division Inhibitor 1 Ameliorates Mitochondrial Injury, Apoptosis, and Motor Dysfunction After Acute Spinal Cord Injury in Rats.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Lipid droplets as redox-active organelles after spinal cord injury: lipid peroxidation, mitochondrial dysfunction, and neuroinflammation.Redox report : communications in free radical research · 2026Review
- Mitochondrial dynamics reveal potential to facilitate axonal regeneration after spinal cord injury.Journal of translational medicine · 2025Review
- Therapeutic potential of EVs loaded with CB2 receptor agonist in spinal cord injury via the Nrf2/HO-1 pathway.Redox report : communications in free radical research · 2024Article
- Ligand-Screened Cerium-Based MOF Microcapsules Promote Nerve Regeneration via Mitochondrial Energy Supply.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mesenchymal Stem Cell-Derived Mitochondria Enhance Extracellular Matrix-Derived Grafts for the Repair of Nerve Defect.Advanced healthcare materials · 2024Article
- Photobiomodulation provides neuroprotection through regulating mitochondrial fission imbalance in the subacute phase of spinal cord injury.Neural regeneration research · 2023Article
- Therapeutic Effect of Mitochondrial Division Inhibitor-1 (Mdivi-1) on Hyperglycemia-Exacerbated Early and Delayed Brain Injuries after Experimental Subarachnoid Hemorrhage.International journal of molecular sciences · 2022Article
- Human Umbilical Cord Mesenchymal Stem Cells Derived Exosomes Promote Neurological Function Recovery in a Rat Spinal Cord Injury Model.Neurochemical research · 2022Article
- Mitochondrial function in spinal cord injury and regeneration.Cellular and molecular life sciences : CMLS · 2022Review
- Lithium promotes long-term neurological recovery after spinal cord injury in mice by enhancing neuronal survival, gray and white matter remodeling, and long-distance axonal regeneration.Frontiers in cellular neuroscience · 2022Article
- Mitochondrial Transplantation Attenuates Neural Damage and Improves Locomotor Function After Traumatic Spinal Cord Injury in Rats.Frontiers in neuroscience · 2022Article
- Trehalose Augments Neuron Survival and Improves Recovery from Spinal Cord Injury via mTOR-Independent Activation of Autophagy.Oxidative medicine and cellular longevity · 2021Article
- Epidural Spinal Cord Stimulation Promotes Motor Functional Recovery by Enhancing Oligodendrocyte Survival and Differentiation and by Protecting Myelin after Spinal Cord Injury in Rats.Neuroscience bulletin · 2020Article
- Article
- Serial plasma DNA levels as predictors of outcome in patients with acute traumatic cervical spinal cord injury.Journal of translational medicine · 2019Article
- Emerging molecular therapeutic targets for spinal cord injury.Expert opinion on therapeutic targets · 2019Review
- Mdivi-1, a mitochondrial fission inhibitor, modulates T helper cells and suppresses the development of experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2019Article
- The effect of 808 nm and 905 nm wavelength light on recovery after spinal cord injury.Scientific reports · 2019Article
- Electroacupuncture and Curcumin Promote Oxidative Balance and Motor Function Recovery in Rats Following Traumatic Spinal Cord Injury.Neurochemical research · 2019Article
- Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction.Theranostics · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial division inhibitor 1 (Mdivi-1) is the most effective pharmacological inhibitor of mitochondrial fission. Spinal cord injury (SCI) is a common and serious trauma, which lacks efficient treatment. This study aimed to detect the role of Mdivi-1 in neuronal injury and its underlying mechanism after acute SCI (ASCI) in rats. Western blot analysis showed that Bax levels on the mitochondrial outer membrane, and release of cytochrome C (cytC) and apoptosis-inducing factor (AIF) from the mitochondria began to increase significantly at 4 h after ASCI, then peaked at 16 h, and declined significantly from 16 to 24 h. However, the mitochondrial levels of Bcl-2 increased significantly at 2 h, peaked at 4 h, and subsequently significantly decreased from 4 to 24 h after ASCI. In addition, Mdivi-1(1.2 mg/kg) significantly suppressed the translocation of dynamin-related protein 1 (Drp1) and Bax to the mitochondria, mitochondrial depolarization, decrease of ATP and reduced Glutathione, increase of the Malondialdehyde, cytC release, and AIF translocation at 16 h and 3 days after ASCI, and also inhibited the caspase-3 activation and decrease of the percentage of apoptotic cells at 16 h, 3 and 10 days, further, ameliorated the motor dysfunction greatly from 3 to 10 days after ASCI in rats. This neuroprotective effect was dose-dependent. However, Mdivi-1(1.2 mg/kg) had no effects on the translocation of Bcl-2 and fission protein 1 on the mitochondria, and did not affect the expression of total Drp1 at 16 h after ASCI. Our experimental findings indicated that Mdivi-1 can protect rats against ASCI, and that its underlying mechanism may be associated with inhibition of Drp1 translocation to the mitochondria, alleviation of mitochondrial dysfunction and oxidative stress, and suppression of caspase-dependent and -independent apoptosis.
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