ArticleMolecular neurobiology2024
Changes of Nuclear Factor Kappa-B Pathway Activity in Hippocampus After Acute Carbon Monoxide Poisoning and Its Role in Nerve Cell Injury.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Inflammatory and metabolic mediators of acute carbon monoxide poisoning: a Mendelian randomization study.World journal of emergency medicine · 2026Article
- Study on the construction of a predictive model for delayed encephalopathy after acute carbon monoxide poisoning.BMC neurology · 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
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Authors and funding
5 authors.
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Abstract
Acute carbon monoxide poisoning (ACOP) causes tissue hypoxia and damage mainly by binding to hemoglobin (Hb). This article aimed to explore the changes in the activity of nuclear factor kappa-B (NF-κB) pathway in the hippocampus after ACOP and its role in nerve cell damage. This article used 30 Sprague-Dawley (SD) rats as the research object, which were randomly divided into two groups, ACOP group and controls. The model of carbon monoxide (CO) poisoning was established, and then the activity of NF-κB pathway in the hippocampus of the two groups of rats was detected, and the statistical analysis was performed. Compared with the controls, the activity of NF-κB pathway in the hippocampus of the ACOP group was significantly increased (P < 0.05). The degree of neuronal damage in the ACOP group was also significantly increased. ACOP increases the activity of the NF-κB pathway in the hippocampus and may cause neuronal damage through this pathway. This provides new ideas and methods for the treatment of ACOP, and also provides new evidence for the role of NF-κB pathway in neuronal injury.
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