ArticleInflammation2016
Erythropoietin Protects Rat Brain Injury from Carbon Monoxide Poisoning by Inhibiting Toll-Like Receptor 4/NF-kappa B-Dependent Inflammatory Responses.
Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- Microparticles Expressing IL-1β Are Linked to Neuroinflammation and Cognitive Decline After Carbon Monoxide Poisoning.International journal of molecular sciences · 2026Article
- Core Neuroinflammatory Pathways Contributing to Delayed Encephalopathy After Acute Carbon Monoxide Poisoning Revealed by Multi-omics and Single Nucleus RNA-Seq.Current medicinal chemistry · 2026Article
- The neutrophil-to-lymphocyte ratio is associated with the frequency of delayed neurologic sequelae in patients with carbon monoxide poisoning.Scientific reports · 2023Article
- Hyperbaric oxygen should be used for carbon monoxide poisoning.British journal of clinical pharmacology · 2023Article
- Early Toll-like receptor 4 inhibition improves immune dysfunction in the hippocampus after hypoxic-ischemic brain damage.International journal of medical sciences · 2022Article
- Combination of autophagy and NFE2L2/NRF2 activation as a treatment approach for neuropathic pain.Autophagy · 2021Article
- Losartan Improves Memory, Neurogenesis and Cell Motility in Transgenic Alzheimer's Mice.Pharmaceuticals (Basel, Switzerland) · 2021Article
- TAK‑242 exerts a neuroprotective effect via suppression of the TLR4/MyD88/TRIF/NF‑κB signaling pathway in a neonatal hypoxic‑ischemic encephalopathy rat model.Molecular medicine reports · 2020Article
- Resatorvid protects against hypoxic-ischemic brain damage in neonatal rats.Neural regeneration research · 2020Article
- The Cannabinoid WIN 55,212-2 Reduces Delayed Neurologic Sequelae After Carbon Monoxide Poisoning by Promoting Microglial M2 Polarization Through ST2 Signaling.Journal of molecular neuroscience : MN · 2020Article
- PEGylated Erythropoietin Protects against Brain Injury in the MCAO-Induced Stroke Model by Blocking NF-κB Activation.Biomolecules & therapeutics · 2020Article
- Article
- Regulation of TLR4 expression mediates the attenuating effect of erythropoietin on inflammation and myocardial fibrosis in rat heart.International journal of molecular medicine · 2018Article
- Pretreatment with Erythropoietin Attenuates Lung Ischemia/Reperfusion Injury via Toll-Like Receptor-4/Nuclear Factor-κB (TLR4/NF-κB) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Ursolic Acid Ameliorates Inflammation in Cerebral Ischemia and Reperfusion Injury PossiblyFrontiers in neurology · 2018Article
- Neuroprotective Effect of Erythropoietin on Phenylhydrazine-Induced Hemolytic Hyperbilirubinemia in Neonatal Rats.Neurochemical research · 2017Article
- 3,4-Dihydroxyphenylethanol alleviates early brain injury by modulating oxidative stress and Akt and nuclear factor-κB pathways in a rat model of subarachnoid hemorrhage.Experimental and therapeutic medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory responses play critical roles in carbon monoxide (CO) poisoning-induced cerebral injury. The present study investigated whether erythropoietin (EPO) modulates the toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) inflammatory signaling pathways in brain injury after acute CO poisoning. EPO (2500 and 5000 U/kg) was injected subcutaneously twice a day after acute CO poisoning for 2 days. At 48 h after treatment, the expression levels of TLR4 and NF-κB as well as the levels of inflammatory cytokines in the hippocampal tissues were measured. Our results showed that CO poisoning induced a significant upregulation of TLR4, NF-κB, and inflammatory cytokines in the injured rat hippocampal tissues. Treatment with EPO remarkably suppressed the gene and protein expression levels of TLR4 and NF-κB, as well as the concentrations of TNF-α, IL-1β, and IL-6 in the hippocampal tissues. EPO treatment ameliorated CO poisoning-induced histological edema and neuronal necrosis. These results suggested that EPO protected against CO poisoning-induced brain damage by inhibiting the TLR4-NF-κB inflammatory signaling pathway.
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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.