ArticleBrain pathology (Zurich, Switzerland)2017
Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia.
Article in Brain pathology (Zurich, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 53 citations in OpenAlex.
- 3',4'-Dihydroxyflavonol has a positive effect on the cerebellum oxidant/antioxidant system and BDNF and transmitter levels in focal brain ischemia-reperfusion.Journal of bioenergetics and biomembranes · 2026Article
- Therapeutic strategies to ameliorate mitochondrial oxidative stress in ischaemia-reperfusion injury: A narrative review.Clinical science (London, England : 1979) · 2025Review
- Dynamics in Redox-Active Molecules Following Ischemic Preconditioning in the Brain.Neurology international · 2024Article
- Research hotspots and frontiers of preconditioning in cerebral ischemia: A bibliometric analysis.Heliyon · 2024Review
- The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus.Cellular and molecular neurobiology · 2023Review
- Article
- The role of SUMOylation in the neurovascular dysfunction after acquired brain injury.Frontiers in pharmacology · 2023Review
- Effects of Brain Factor‑7® against motor deficit and oxidative stress in a mouse model of MPTP‑induced Parkinson's disease.Experimental and therapeutic medicine · 2022Article
- Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and HAntioxidants (Basel, Switzerland) · 2022Article
- Fermented Mentha arvensis administration provides neuroprotection against transient global cerebral ischemia in gerbils and SH-SY5Y cells via downregulation of the MAPK signaling pathway.BMC complementary medicine and therapies · 2022Article
- α-tocopherol pretreatment alleviates cerebral ischemia-reperfusion injury in rats.CNS neuroscience & therapeutics · 2022Article
- Hypothermia Induced by Oxcarbazepine after Transient Forebrain Ischemia Exerts Therapeutic Neuroprotection through Transient Receptor Potential Vanilloid Type 1 and 4 in Gerbils.International journal of molecular sciences · 2021Article
- Therapeutic Effects of Risperidone against Spinal Cord Injury in a Rat Model of Asphyxial Cardiac Arrest: A Focus on Body Temperature, Paraplegia, Motor Neuron Damage, and Neuroinflammation.Veterinary sciences · 2021Article
- Neuroprotective effects and mechanisms of ischemic/hypoxic preconditioning on neurological diseases.CNS neuroscience & therapeutics · 2021Review
- Article
- Comparison of age-dependent alterations in thioredoxin 2 and thioredoxin reductase 2 expressions in hippocampi between mice and rats.Laboratory animal research · 2021Article
- Neuroprotective Effect of Astragaloside IV on Cerebral Ischemia/Reperfusion Injury Rats Through Sirt1/Mapt Pathway.Frontiers in pharmacology · 2021Article
- miR-214 Alleviates Ischemic Stroke-Induced Neuronal Death by Targeting DAPK1 in Mice.Frontiers in neuroscience · 2021Article
- PycnogenolNutrients · 2020Article
- Laminarin Pretreatment Provides Neuroprotection against Forebrain Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Neuroinflammation in Aged Gerbils.Marine drugs · 2020Article
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13 authors at 5 institutions in 1 country.
Funding
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Abstract
Preconditioning by brief ischemic episode induces tolerance to a subsequent lethal ischemic insult, and it has been suggested that reactive oxygen species are involved in this phenomenon. Thioredoxin 2 (Trx2), a small protein with redox-regulating function, shows cytoprotective roles against oxidative stress. Here, we had focused on the role of Trx2 in ischemic preconditioning (IPC)-mediated neuroprotection against oxidative stress followed by a subsequent lethal transient cerebral ischemia. Animals used in this study were randomly assigned to six groups; sham-operated group, ischemia-operated group, IPC plus (+) sham-operated group, IPC + ischemia-operated group, IPC + auranofin (a TrxR2 inhibitor) + sham-operated group and IPC + auranofin + ischemia-operated group. IPC was subjected to a 2 minutes of sublethal transient ischemia 1 day prior to a 5 minutes of lethal transient ischemia. A significant loss of neurons was found in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) in the ischemia-operated-group 5 days after ischemia-reperfusion; in the IPC + ischemia-operated-group, pyramidal neurons in the SP were well protected. In the IPC + ischemia-operated-group, Trx2 and TrxR2 immunoreactivities in the SP and its protein level in the CA1 were not significantly changed compared with those in the sham-operated-group after ischemia-reperfusion. In addition, superoxide dismutase 2 (SOD2) expression, superoxide anion radical ( O2-) production, denatured cytochrome c expression and TUNEL-positive cells in the IPC + ischemia-operated-group were similar to those in the sham-operated-group. Conversely, the treatment of auranofin to the IPC + ischemia-operated-group significantly increased cell damage/death and abolished the IPC-induced effect on Trx2 and TrxR2 expressions. Furthermore, the inhibition of Trx2R nearly cancelled the beneficial effects of IPC on SOD2 expression, O2- production, denatured cytochrome c expression and TUNEL-positive cells. In brief, this study shows that IPC conferred neuroprotection against ischemic injury by maintaining Trx2 and suggests that the maintenance or enhancement of Trx2 expression by IPC may be a legitimate strategy for therapeutic intervention of cerebral ischemia.
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