ArticleNeurochemical research2010
Spatio-temporal distribution of inflammatory reaction and expression of TLR2/4 signaling pathway in rat brain following permanent focal cerebral ischemia.
Article in Neurochemical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Method parameters' impact on mortality and variability in rat stroke experiments: a meta-analysis.BMC neuroscience · 2013Pooled it
- Ischemic stroke and intervention strategies based on the timeline of stroke progression: Review and prospects.Acta pharmaceutica Sinica. B · 2025Review
- Detrimental influence of Arginase-1 in infiltrating macrophages on poststroke functional recovery and inflammatory milieu.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Distinct trajectory patterns of neutrophil-to-albumin ratio predict clinical outcomes after endovascular therapy in large vessel occlusion stroke.Frontiers in aging neuroscience · 2025Article
- Rodent ischemic stroke models and their relevance in preclinical research.Neuroprotection (Chichester, England) · 2024Review
- Day 3 neutrophil-to-lymphocyte ratio and its derived indices predict 90-day poor outcomes following mechanical thrombectomy in acute ischemic stroke patients.Frontiers in neurology · 2024Article
- Neuroinflammatory Biomarkers in the Brain, Cerebrospinal Fluid, and Blood After Ischemic Stroke.Molecular neurobiology · 2023Review
- Inhibition of the NLRP3 Inflammasome Activation/Assembly through the Activation of the PI3K Pathway by Naloxone Protects Neural Stem Cells from Ischemic Condition.Molecular neurobiology · 2023Article
- Emerging Targets for Modulation of Immune Response and Inflammation in Stroke.Neurochemical research · 2023Review
- Toll-like receptors in pathogenesis of neurodegenerative diseases and their therapeutic potential.Immunity, inflammation and disease · 2023Review
- Day 1 neutrophil-to-lymphocyte ratio (NLR) predicts stroke outcome after intravenous thrombolysis and mechanical thrombectomy.Frontiers in neurology · 2022Article
- Attenuation of the Induction of TLRs 2 and 4 Mitigates Inflammation and Promotes Neurological Recovery After Focal Cerebral Ischemia.Translational stroke research · 2021Article
- Persistent inflammation worsens short-term outcomes in massive stroke patients.BMC neurology · 2021Article
- Mesencephalic Electrical Stimulation Reduces Neuroinflammation after Photothrombotic Stroke in Rats by Targeting the Cholinergic Anti-Inflammatory Pathway.International journal of molecular sciences · 2021Article
- Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review.Frontiers in pharmacology · 2021Review
- Biological Functions and Regulatory Mechanisms of Hypoxia-Inducible Factor-1α in Ischemic Stroke.Frontiers in immunology · 2021Review
- XingNaoJing injection ameliorates cerebral ischaemia/reperfusion injury via SIRT1-mediated inflammatory response inhibition.Pharmaceutical biology · 2020Article
- Toll-Like Receptor 4 Signaling in Focal Cerebral Ischemia: a Focus on the Neurovascular Unit.Molecular neurobiology · 2020Review
- The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury.Frontiers in cellular neuroscience · 2020Review
- Early toll-like receptor 4 blockade reduces ROS and inflammation triggered by microglial pro-inflammatory phenotype in rodent and human brain ischaemia models.British journal of pharmacology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are considered to mediate the inflammatory reaction, which are involved in the pathophysiological processes of cerebral ischemia injury. To elucidate the possible role of inflammatory reaction and TLR2/4 signaling pathway in cerebral ischemia, in the present study, we explored the spatio-temporal distribution of inflammatory reaction, and further investigated the time-course expression of TLR2/4 and the downstream effector molecules after focal cerebral ischemia in rats. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO) for 6, 12, 24, 48 and 72 h. Neurological deficit, cerebral infarction and neutrophil infiltration were measured at different time points following pMCAO. Expression of TLR2/4 were examined by immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Nuclear factor-kappaB (NF-kappaB) and cyclooxygenase-2 (COX-2) were determined by western blot. Serum content of tumor necrosis factor-alpha (TNF-alpha) was detected by enzyme-linked immunosorbent assay (ELISA). Experimental results showed that pMCAO caused an increase of neutrophil infiltration in infarcted brain tissue, with a peaked activity at 24 h of ischemia. The inflammatory molecules including TLR2, TLR4, NF-kappaB, COX-2 and TNF-alpha were significantly increased after pMCAO, especially during 12-24 h of ischemia, which were correlated with pMCAO-induced brain injury and cerebral inflammation. Our studies suggested that TLR2/4 signaling pathway likely aggravated ischemic brain injury through mediating the inflammatory reaction. TLR2/4 signaling pathway may be a promising therapeutic target for cerebral ischemia injury.
Indexed as
Identifiers
What OpenQuestion holds
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.