ArticleCNS neuroscience & therapeutics2013
Transient lack of glucose but not O2 is involved in ischemic postconditioning-induced neuroprotection.
Article in CNS neuroscience & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Neuroprotective Role of Acidosis in Ischemia: Review of the Preclinical Evidence.Molecular neurobiology · 2021Pooled it
- Urolithin A-activated autophagy but not mitophagy protects against ischemic neuronal injury by inhibiting ER stress in vitro and in vivo.CNS neuroscience & therapeutics · 2019Article
- Ischaemic and hypoxic conditioning: potential for protection of vital organs.Experimental physiology · 2019Review
- Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia.Journal of visualized experiments : JoVE · 2017Article
- PARK2-dependent mitophagy induced by acidic postconditioning protects against focal cerebral ischemia and extends the reperfusion window.Autophagy · 2017Article
- Bakkenolide-IIIa Protects Against Cerebral Damage Via Inhibiting NF-κB Activation.CNS neuroscience & therapeutics · 2015Article
- Inhibition of G protein-coupled receptor 81 (GPR81) protects against ischemic brain injury.CNS neuroscience & therapeutics · 2015Article
- Article
- Extracellular visfatin has nicotinamide phosphoribosyltransferase enzymatic activity and is neuroprotective against ischemic injury.CNS neuroscience & therapeutics · 2014Article
- A novel neuroprotective strategy for ischemic stroke: transient mild acidosis treatment by CO2 inhalation at reperfusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Platelet-derived microparticles are implicated in remote ischemia conditioning in a rat model of cerebral infarction.CNS neuroscience & therapeutics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimCerebral ischemic postconditioning has emerged recently as a kind of endogenous strategy for neuroprotection. We set out to test whether hypoxia or glucose deprivation (GD) would substitute for ischemia in postconditioning.
methodsAdult male C57BL/6J mice were treated with postconditioning evoked by ischemia (bilateral common carotid arteries occlusion) or hypoxia (8% O(2) ) after 45-min middle cerebral arterial occlusion. Corticostriatal slices from mice were subjected to 1-min oxygen-glucose deprivation (OGD), GD, or oxygen deprivation (OD) postconditioning at 5 min after 15-min OGD.
resultsHypoxic postconditioning did not decrease infarct volume or improve neurologic function at 24 h after reperfusion, while ischemic postconditioning did. Similarly, OGD and GD but not OD postconditioning attenuated the OGD/reperfusion-induced injury in corticostriatal slices. The effective duration of low-glucose (1 mmol/L) postconditioning was longer than that of OGD postconditioning. Moreover, OGD and GD but not OD postconditioning reversed the changes of glutamate, GABA, glutamate transporter-1 protein expression, and glutamine synthetase activity induced by OGD/reperfusion.
conclusionsThese results suggest that the transient lack of glucose but not oxygen plays a key role in ischemic postconditioning-induced neuroprotection, at least partly by regulating glutamate metabolism. Low-glucose postconditioning might be a clinically safe and feasible therapeutic approach against cerebral ischemia/reperfusion injury.
Indexed as
Identifiers
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.