ArticleMediators of inflammation2012
Biphasic activation of nuclear factor-kappa B in experimental models of subarachnoid hemorrhage in vivo and in vitro.
Article in Mediators of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- ITF2357 regulates NF-κB signaling pathway to protect barrier integrity in retinal pigment epithelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- miR-452-3p Targets HDAC3 to Inhibit p65 Deacetylation and Activate the NF-κB Signaling Pathway in Early Brain Injury after Subarachnoid Hemorrhage.Neurocritical care · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Adiantum capillus-veneris Linn protects female reproductive system against carbendazim toxicity in rats: immunohistochemical, histopathological, and pathophysiological studies.Environmental science and pollution research international · 2021Article
- Biphasic activation of nuclear factor-κB and expression of p65 and c-Rel following traumatic neuronal injury.International journal of molecular medicine · 2018Article
- Cooperation of Rel family members in regulating AβCell death & disease · 2017Article
- Pentoxifylline Alleviates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats: Possibly via Inhibiting TLR 4/NF-κB Signaling Pathway.Neurochemical research · 2017Article
- Inhibition of the Receptor for Advanced Glycation End-Products (RAGE) Attenuates Neuroinflammation While Sensitizing Cortical Neurons Towards Death in Experimental Subarachnoid Hemorrhage.Molecular neurobiology · 2017Article
- Recombinant human brain-derived neurotrophic factor prevents neuronal apoptosis in a novel in vitro model of subarachnoid hemorrhage.Neuropsychiatric disease and treatment · 2017Article
- Increased Expression of Caspase-12 After Experimental Subarachnoid Hemorrhage.Neurochemical research · 2016Article
- Hydrogen-Rich Saline Attenuated Subarachnoid Hemorrhage-Induced Early Brain Injury in Rats by Suppressing Inflammatory Response: Possible Involvement of NF-κB Pathway and NLRP3 Inflammasome.Molecular neurobiology · 2016Article
- Rutin Inhibits Neuroinflammation and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage, Possibly Through Suppressing the RAGE-NF-κB Inflammatory Signaling Pathway.Neurochemical research · 2016Article
- Neurovascular events after subarachnoid hemorrhage: focusing on subcellular organelles.Acta neurochirurgica. Supplement · 2015Review
- Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro.Journal of neuroinflammation · 2014Article
- Expression and cell distribution of neuroglobin in the brain tissue after experimental subarachnoid hemorrhage in rats: a pilot study.Cellular and molecular neurobiology · 2014Article
- Biphasic activation of nuclear factor kappa B and expression of p65 and c-Rel after traumatic brain injury in rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proven that nuclear factor-kappa B (NF-κB) is activated as a well-known transcription factor after subarachnoid hemorrhage (SAH). However, the panoramic view of NF-κB activity after SAH remained obscure. Cultured neurons were signed into control group and six hemoglobin- (Hb-) incubated groups. One-hemorrhage rabbit SAH model was produced, and the rabbits were divided randomly into one control group and five SAH groups. NF-κB activity was detected by electrophoretic mobility shift assay (EMSA) and immunohistochemistry. Real-time polymerase chain reaction (PCR) was performed to assess the downstream genes of NF-κB. NeuN immunofluorescence and lactate dehydrogenase (LDH) quantification were used to estimate the neuron injury. Double drastically elevated NF-κB activity peaks were detected in rabbit brains and cultured neurons. The downstream gene expressions showed an accordant phase peaks. NeuN-positive cells decreased significantly in day 3 and day 10 groups. LDH leakage exhibited a significant increase in Hb-incubated groups, but no significant difference was found between the Hb incubated groups. These results suggested that biphasic increasing of NF-κB activity was induced after SAH, and the early NF-κB activity peak indicated the injury role on neurons; however, the late peak might not be involved in the deteriorated effect on neurons.
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