ArticleJournal of orthopaedic surgery and research2023
Diallyl trisulfide improves spinal cord ischemia-reperfusion injury damage by activating AMPK to stabilize mitochondrial function.
Article in Journal of orthopaedic surgery and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Exercise training promotes nerve cell repair and regeneration after spinal cord injury.Neural regeneration research · 2026Article
- Garlic-derived bioactive components in neuropathic pain: molecular mechanisms and therapeutic promise.Frontiers in molecular neuroscience · 2026Review
- The Therapeutic Potential of Garlic-Derived Organic Polysulfides for Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSpinal cord ischemia-reperfusion injury (SCII) is a catastrophic event, which can cause paraplegia in severe cases. In the reperfusion stage, oxidative stress was up-regulated, which aggravated the injury and apoptosis of neurons. As the main active ingredient of garlic, diallyl trisulfide (DATS) displays strong antioxidant capacity. However, it is unknown whether DATS can protect the neurons of SCII. MATERIALS AND
methodsIn this study, the descending aorta at the distal end of the left subclavian artery was ligated and perfused again after 14 min. Samples including blood and spinal cord (L2-L5) were taken 24 h later for morphological and biochemical examination.
resultsAfter SCII, the rats showed motor dysfunction, increase apoptosis, malondialdehyde content, mitochondrial biogenesis and dynamic balance disorder. After the application of DATS, the adenosine monophosphate activated protein kinase (AMPK) was activated, the mitochondrial damage was improved, the oxidative stress was weakened, and the neuronal damage was recovered to some extent. However, the addition of compound C significantly weakened the protective effect of DATS.
conclusionOxidative stress caused by mitochondrial damage was one of the important mechanisms of neuronal damage in SCII. DATS could activate AMPK, stabilize mitochondrial biogenesis and dynamic balance, and reduce neuronal damage caused by oxidative stress.
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Registered trials
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