ArticleNeural regeneration research2013
Effect of minocycline on cerebral ischemia-reperfusion injury.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Filling the gaps on stroke research: Focus on inflammation and immunity.Brain, behavior, and immunity · 2021Review
- Therapeutic Effects of Minocycline Pretreatment in the Locomotor and Sensory Complications of Spinal Cord Injury in an Animal Model.Journal of molecular neuroscience : MN · 2020Article
- Neuroprotective effects of minocycline on focal cerebral ischemia injury: a systematic review.Neural regeneration research · 2020Review
- The anti-inflammatory effect of minocycline on endotoxin-induced uveitis and retinal inflammation in rats.Molecular vision · 2019Article
- Combination therapy of human bone marrow-derived mesenchymal stem cells and minocycline improves neuronal function in a rat middle cerebral artery occlusion model.Stem cell research & therapy · 2018Article
- Minocycline modulates microglia polarization in ischemia-reperfusion model of retinal degeneration and induces neuroprotection.Scientific reports · 2017Article
- Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage.Molecular neurobiology · 2016Article
Corrections and comments
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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
Minocylcine, a tetracycline derivate, has been shown to cross the blood-brain barrier and enter the central nervous system. In this study, cerebral ischemia-reperfusion injury models were established using the suture method, and minocycline was immediately injected intraperitoneally after cerebral ischemia-reperfusion (22.5 mg/kg, initially 45 mg/kg) at a 12-hour interval. Results showed that after minocycline treatment, the volume of cerebral infarction was significantly reduced, the number of surviving cell in the hippocampal CA1 region increased, the number of apoptotic cells decreased, the expression of caspase-3 and poly(adenosine diphosphate-ribose) polymerase-1 protein was down-regulated, and the escape latency in the water maze test was significantly shortened compared with the ischemia-reperfusion group. Our experimental findings indicate that minocycline can protect against neuronal injury induced by focal ischemia-reperfusion, which may be mediated by the inhibition of caspase-3 and poly(adenosine diphosphate-ribose) polymerase-1 protein expression.
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What OpenQuestion holds
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.