ArticleNeuroreport2019
Role of the Janus kinase 2/signal transducers and activators of transcription 3 pathway in the protective effect of remote ischemia preconditioning against cerebral ischemia-reperfusion injury in rats.
Article in Neuroreport, 2019. 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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Preclinical evidence of remote ischemic conditioning in ischemic stroke, a metanalysis update.Scientific reports · 2021Pooled it
- Mechanisms and Therapeutic Targets of Ischemia-Reperfusion Injury in Stroke: A Narrative Review Focusing on Blood-Brain Barrier Dysfunction.Brain sciences · 2026Review
- Unveiling the neuroprotective power: the role of autophagy in remote ischemic conditioning.Metabolic brain disease · 2025Review
- Exercise preconditioning attenuates cerebral ischemia-induced neuronal apoptosis, Th17/Treg imbalance, and inflammation in rats by inhibiting the JAK2/STAT3 pathway.Brain and behavior · 2023Article
- A Machine Learning-Based Classification of Immunogenic Cell Death Regulators and Characterisation of Immune Microenvironment in Acute Ischemic Stroke.International journal of clinical practice · 2023Article
- Construction of a Joint Prediction Model for the Occurrence of Ischemic Stroke and Acute Myocardial Infarction Based on Bioinformatic Analysis.Disease markers · 2022Article
- Acupuncture protects against cerebral ischemia-reperfusion injury via suppressing endoplasmic reticulum stress-mediated autophagy and apoptosis.Molecular medicine (Cambridge, Mass.) · 2020Article
- Article
- Eugenol Attenuates Cerebral Ischemia-Reperfusion Injury by Enhancing AutophagyFrontiers in pharmacology · 2020Article
- Neuroprotective potential of imatinib in global ischemia-reperfusion-induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- The mechanism and tumor inhibitory study of Lagopsis supine ethanol extract on colorectal cancer in nude mice.BMC complementary and alternative medicine · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remote ischemia preconditioning (RIPC) is a convenient and effective method for alleviating cerebral ischemia-reperfusion injury (CIRI). However, to date, the underlying mechanism has not been fully elucidated. The aim of this research was to explore the protective mechanism of RIPC on the brain after CIRI. Four groups of rats were included in this experiment: the sham group, the middle cerebral artery occlusion (MCAO) group, the RIPC group, and the AG490 group. As an inhibitor of Janus kinase 2 (JAK2), AG490 was used after MCAO in the AG490 group to explore the role of JAK2/signal transducers and activators of transcription 3 (STAT3) after CIRI. Brain tissue was collected for evaluation after 2 h of ischemia and 24 h of reperfusion. ELISA for interleukin (IL)-6, IL-1β and tumor necrosis factor-α, western blot for phosphorylated-JAK2 and phosphorylated-STAT3, the neurological severity score and Longa scoring system for neurological deficit evaluation, triphenyltetrazolium chloride staining for cerebral infarction, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining for apoptotic cells in the brain tissue were performed. Neurological function in the RIPC group was notably better than that in the MCAO group. There were smaller infarction sizes and fewer apoptotic cells in the ischemic area in the RIPC group than in the MCAO group. In the RIPC group, the expression levels of IL-1β, tumor necrosis factor-α, IL-6, and phosphorylated-JAK2 and phosphorylated-STAT3 were significantly lower than those in the MCAO group. The findings in the RIPC and AG490 groups were similar. The inflammatory response and apoptosis are two important processes involved in brain dysfunction after CIRI. The JAK2/STAT3 signaling pathway has an underlying relationship with these two processes. These findings suggest that RIPC can alleviate the damage to brain tissue by CIRI by regulating the JAK2/STAT3 signaling pathway negatively.
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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.