ArticleNeural regeneration research2014
Inflammatory response and neuronal necrosis in rats with cerebral ischemia.
Article in Neural regeneration research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Rutaecarpine Attenuates Oxidative Stress-Induced Traumatic Brain Injury and Reduces Secondary InjuryFrontiers in pharmacology · 2022Article
- Pathways Involved in Remyelination after Cerebral Ischemia.Current neuropharmacology · 2022Article
- The Effect of theFrontiers in neurology · 2021Article
- Cholinergic Modulation of Glial Function During Aging and Chronic Neuroinflammation.Frontiers in cellular neuroscience · 2020Review
- The role of intestinal endotoxemia in a rat model of aluminum neurotoxicity.Molecular medicine reports · 2017Article
- Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury.Scientific reports · 2017Article
- Mesenchymal stem cells protect neurons against hypoxic-ischemic injury via inhibiting parthanatos, necroptosis, and apoptosis, but not autophagy.Cellular and molecular neurobiology · 2017Article
- Neuroprotective effect of angiotensin II type 2 receptor during cerebral ischemia/reperfusion.Neural regeneration research · 2016Article
- Melatonin and Ischemic Stroke: Mechanistic Roles and Action.Advances in pharmacological sciences · 2015Review
- Effects of Etanercept against Transient Cerebral Ischemia in Diabetic Rats.BioMed research international · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the middle cerebral artery occlusion model of ischemic injury, inflammation primarily occurs in the infarct and peripheral zones. In the ischemic zone, neurons undergo necrosis and apoptosis, and a large number of reactive microglia are present. In the present study, we investigated the pathological changes in a rat model of middle cerebral artery occlusion. Neuronal necrosis appeared 12 hours after middle cerebral artery occlusion, and the peak of neuronal apoptosis appeared 4 to 6 days after middle cerebral artery occlusion. Inflammatory cytokines and microglia play a role in damage and repair after middle cerebral artery occlusion. Serum intercellular cell adhesion molecule-1 levels were positively correlated with the permeability of the blood-brain barrier. These findings indicate that intercellular cell adhesion molecule-1 may be involved in blood-brain barrier injury, microglial activation, and neuronal apoptosis. Inhibiting blood-brain barrier leakage may alleviate neuronal injury following ischemia.
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Registered trials
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.