ArticleExperimental and therapeutic medicine2016
Effects of erythropoietin preconditioning on rat cerebral ischemia-reperfusion injury and the GLT-1/GLAST pathway.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- The mTOR/Akt pathway is involved in regulating astrocyte growth and GLT-1 expression during cerebral ischemia-reperfusion.PloS one · 2026Article
- Astrocyte-Neuron Metabolic Synergies in Neurological Homeostasis and Disease.Neurochemical research · 2025Review
- Expression of erythropoietin receptor protein in the mouse hippocampus in response to normobaric hypoxia.Heliyon · 2024Article
- Unravelling the potential neuroprotective facets of erythropoietin for the treatment of Alzheimer's disease.Metabolic brain disease · 2022Review
- Neuroprotective effects of EpoL against oxidative stress induced by soluble oligomers of Aβ peptide.Redox biology · 2019Article
- Upregulation of GLT-1 via PI3K/Akt Pathway Contributes to Neuroprotection Induced by Dexmedetomidine.Frontiers in neurology · 2019Article
- Neuroprotective effects of erythropoietin on neurodegenerative and ischemic brain diseases: the role of erythropoietin receptor.Neural regeneration research · 2017Review
- Erythropoietin Pretreatment Effect on Blood Glucose and Its Relationship With Inflammatory Factors After Brain Ischemic-Reperfusion Injury in Rats.Basic and clinical neuroscienceArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate whether erythropoietin (EPO) preconditioning affects the expression of glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST) and protects against rat cerebral ischemia-reperfusion injury. A total of 140 Sprague Dawley rats were randomly assigned to one of the following four groups: Sham, EPO-sham, middle cerebral artery occlusion (MCAO) and EPO-MCAO. Neurological function scores were obtained 24, 36 and 72 h after reperfusion. Seventy-two hours after the induction of cerebral ischemia-reperfusion, the number of apoptotic neural cells and the cerebral infarct volume of each group were measured. The mRNA levels of GLT-1 and GLAST were determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis, while the GLT-1 and GLAST protein levels were assessed using western blotting. The cerebral infarct volume was significantly increased in the MCAO group compared with that in the sham group (P<0.01); however, the infarct volume of the EPO-MCAO group was significantly lower than that of the MCAO group (P<0.01). In addition, the number of apoptotic cells found in the MCAO group was higher than that in the sham group (P<0.01), but the number of apoptotic cells in the EPO-MCAO group was significantly lower than that in the MCAO group (P<0.01). The GLT-1 and GLAST mRNA and protein levels were significantly decreased 72 h after the cerebral ischemia-reperfusion (P<0.01) compared with those in the sham group, whereas the same levels were increased significantly in the EPO-MCAO group relative to those in the MCAO group (P<0.01). In conclusion, EPO preconditioning protected against cerebral ischemia-reperfusion injury and upregulated the GLT-1 and GLAST expression.
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