ArticleMolecular biology reports2013
Remifentanil preconditioning alleviating brain damage of cerebral ischemia reperfusion rats by regulating the JNK signal pathway and TNF-α/TNFR1 signal pathway.
Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
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- A narrative review of neuroprotective effects of remifentanil: from basic research to clinical practice.Frontiers in neurology · 2025Review
- Effects of ischemic postconditioning and long non-coding RNAs in ischemic stroke.Bioengineered · 2022Review
- Opioids Preconditioning Upon Renal Function and Ischemia-Reperfusion Injury: A Narrative Review.Medicina (Kaunas, Lithuania) · 2019Review
- Indispensable role of β-arrestin2 in the protection of remifentanil preconditioning against hepatic ischemic reperfusion injury.Scientific reports · 2019Article
- Treatment of Surgical Brain Injury by Immune Tolerance Induced by Peripheral Intravenous Injection of Biotargeting Nanoparticles Loaded With Brain Antigens.Frontiers in immunology · 2019Article
- Beneficial Effects of Remifentanil Against Excitotoxic Brain Damage in Newborn Mice.Frontiers in neurology · 2019Article
- Remifentanil upregulates hepatic IL-18 binding protein (IL-18BP) expression through transcriptional control.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Immune Tolerance Therapy: A New Method for Treatment of Traumatic Brain Injury.Chinese medical journal · 2018Review
- Treatment of surgical brain injury by immune tolerance induced by intrathymic and hepatic portal vein injection of brain antigens.Scientific reports · 2016Article
- Time-dependent variation of pathways and networks in a 24-hour window after cerebral ischemia-reperfusion injury.BMC systems biology · 2015Article
- Neuroprotective effect of pretreatment with ganoderma lucidum in cerebral ischemia/reperfusion injury in rat hippocampus.Neural regeneration research · 2014Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor (TNF) and the TNF receptor (TNFR) superfamily play very important roles for cell death as well as normal immune regulation. Previous studies have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. The purpose of this investigation was to examine the protective effect of remifentanil preconditioning in cerebral ischemia/reperfusion injury (CIR) and its possible molecular mechanism. Results showed that Remifentanil pretreatment significantly decreased the CD4(+) and increased the CD8(+) in cerebral tissues. Additionally, CD4(+)/CD8(+) in CIR + Remifentanil group was markedly lower than that in CIR group. TNF-α and TNFR1 in CIR + Remifentanil group rats was found to be significant lower than that in CIR group rats. The expression levels of Cyt-c, caspase-3, caspase-9 and pJNK proteins in brain of CIR + Remifentanil group rats were found to significantly decreased compared to CIR group rats. In addition, decreased ROS level indirectly inhibit JNK activation and cell death in CIR rat receiving Remifentanil preconditioning. From current experiment results, at least two signal pathways involve into the process of Remifentanil preconditioning inhibiting cerebral damage induced by ischemia reperfusion. The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-α/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-α/TNFR1, JNK signal pathways. Taken together, this study indicated that regulation of the TNF-α/TNFR1 and JNK signal pathways may provide a new therapy for cerebral damage induced by ischemia and reperfusion.
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