ArticleNeurochemical research2011
Time-course alterations of Toll-like receptor 4 and NF-κB p65, and their co-expression in the gerbil hippocampal CA1 region after transient cerebral ischemia.
Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and HAntioxidants (Basel, Switzerland) · 2022Article
- Fermented Mentha arvensis administration provides neuroprotection against transient global cerebral ischemia in gerbils and SH-SY5Y cells via downregulation of the MAPK signaling pathway.BMC complementary medicine and therapies · 2022Article
- Article
- Neuroprotective Effects of Purpurin Against Ischemic Damage via MAPKs, Bax, and Oxidative Stress Cascades in the Gerbil Hippocampus.Molecular neurobiology · 2022Article
- [D-AlaMediators of inflammation · 2021Article
- Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils.Marine drugs · 2020Article
- Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia.Neural regeneration research · 2019Article
- Time-Course Changes and New Expressions of MIP-3α and Its Receptor, CCR6, in the Gerbil Hippocampal CA1 Area Following Transient Global Cerebral Ischemia.Neurochemical research · 2018Article
- Primary cilia modulate TLR4-mediated inflammatory responses in hippocampal neurons.Journal of neuroinflammation · 2017Article
- Hydroxysafflor Yellow A Attenuates Neuron Damage by Suppressing the Lipopolysaccharide-Induced TLR4 Pathway in Activated Microglial Cells.Cellular and molecular neurobiology · 2016Article
- A possible role of microglia-derived nitric oxide by lipopolysaccharide in activation of astroglial pentose-phosphate pathway via the Keap1/Nrf2 system.Journal of neuroinflammation · 2016Article
- Neuroimmune signaling: a key component of alcohol abuse.Current opinion in neurobiology · 2013Review
- Adolescent morphine exposure affects long-term microglial function and later-life relapse liability in a model of addiction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Neuronal Toll-like receptor 4 signaling induces brain endothelial activation and neutrophil transmigration in vitro.Journal of neuroinflammation · 2012Article
- TLR4 Signaling Selectively and Directly Promotes CGRP Release from Vagal Afferents in the Mouse.eNeuroArticle
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate immune system is very important to modulate the host defense against a large variety of pathogens. Toll-like receptors (TLRs) play a key role in controlling innate immune response. Among TLRs, TLR4 is a specific receptor for lipopolysaccharide and associated with the release of pro-inflammatory cytokines. In the present study, we investigated ischemia-related changes of TLR4 immunoreactivity and its protein level, and nuclear factor κB (NF-κB) p65 immunoreactivity regarding inflammatory responses in the hippocampal CA1 region after 5 min of transient cerebral ischemia to identify the correlation between transient ischemia and inflammation. In the sham-operated group, TLR4 immunoreactivity was easily detected in pyramidal neurons of the hippocampal CA1 region (CA1). TLR4 immunoreactivity in pyramidal neurons was distinctively decreased after ischemia/reperfusion (I/R); instead, based on double immunofluorescence study, TLR4 immunoreactivity was expressed in non-pyramidal neurons and astrocytes from 2 days postischemia. In addition, TLR4 protein level was lowest at 1 day postischemia and highest 4 days after I/R. On the other hand, NF-κB p65 immunoreactivity was not detected in the CA1 of the sham-operated group, and NF-κB p65 immunoreactivity was not observed until 1 day after I/R. However, NF-κB p65 immunoreactivity began to be expressed in astrocytes at 2 days postischemia, and the immunoreactivity was strong 4 days postischemia. Our results indicate that TLR4 and NF-κB p65 immunoreactivity are changed in CA1 pyramidal neurons and newly expressed in astrocytes, not in microglia, in the CA1 region after transient cerebral ischemia.
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