ArticleScientific reports2023
Effects of different remote ischemia perconditioning methods on cerebral infarct volume and neurological impairment in rats.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Reduced Cerebral Infarct Volume in Young UCP2Cells · 2026Article
- Remote Ischemic Preconditioning Exerts Neuroprotective Effects Via the PGC-1α/FNDC5/BDNF Pathway in Focal Brain Ischemia of Rats.Translational stroke research · 2026Article
- Neuroprotective potential of phloroglucinol in focal cerebral ischemia in rats: a mechanistic study.Metabolic brain disease · 2026Article
- Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Detection, Isolation and Quantification of Myocardial Infarct with Four Different Histological Staining Techniques.Diagnostics (Basel, Switzerland) · 2024Article
- Detection, Isolation and Quantification of Myocardial Infarct with Four Different Histological Staining Techniques.bioRxiv : the preprint server for biology · 2024Article
- Article
- Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress.Experimental and therapeutic medicine · 2024Article
- Alpha-pinene modulates inflammatory response and protects against brain ischemia via inducible nitric oxide synthase-nuclear factor-kappa B-cyclooxygenase-2 pathway.Molecular biology reports · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remote ischemic perconditioning (RIPerC) is a novel neuroprotective method against cerebral infarction that has shown efficacy in animal studies but has not been consistently neuroprotective in clinical trials. We focused on the temporal regulation of ischemia-reperfusion by RIPerC to establish an optimal method for RIPerC. Rats were assigned to four groups: 10 min ischemia, 5 min reperfusion; 10 min ischemia, 10 min reperfusion; 5 min ischemia, 10 min reperfusion; and no RIPerC. RIPerC interventions were performed during ischemic stroke, which was induced by a 60-min left middle cerebral artery occlusion. Infarct volume, sensorimotor function, neurological deficits, and cellular expressions of brain-derived neurotrophic factor (BDNF), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and caspase 3 were evaluated 48 h after the induction of ischemia. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) was also performed. RIPerC of 10 min ischemia/10 min reperfusion, and 5 min ischemia/10 min reperfusion decreased infarct volume, improved sensorimotor function, decreased Bax, caspase 3, and TUNEL-positive cells, and increased BDNF and Bcl-2 expressions. Our findings suggest RIPerC with a reperfusion time of approximately 10 min exerts its neuroprotective effects via an anti-apoptotic mechanism. This study provides important preliminary data to establish more effective RIPerC interventions.
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