ArticleScientific reports2016
Interference with Protease-activated Receptor 1 Alleviates Neuronal Cell Death Induced by Lipopolysaccharide-Stimulated Microglial Cells through the PI3K/Akt Pathway.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Activation of PI3K/Akt/HIF-1α Signaling is Involved in Lung Protection of Dexmedetomidine in Patients Undergoing Video-Assisted Thoracoscopic Surgery: A Pilot Study.Drug design, development and therapy · 2020Trial
- PAR-1 in Alzheimer's Disease: Pathophysiological Insights and Mechanistic Perspectives.Current medical science · 2026Review
- Anti-Neuroinflammatory Effects of a Representative Low-Molecular-Weight Component Isolated fromMarine drugs · 2026Article
- Lactoferrin alleviates the adverse effects of early-life inflammation on depression in adults by regulating the activation of microglia.Molecular medicine (Cambridge, Mass.) · 2025Article
- Dexmedetomidine directly binds to and inhibits Toll-like receptor 4.International immunopharmacology · 2024Article
- Long-term GABA Supplementation Regulates Diabetic Gastroenteropathy through GABA Receptor/trypsin-1/PARs/Akt/COX-2 Axis.Doklady. Biochemistry and biophysics · 2024Article
- Receptors on Microglia.Advances in neurobiology · 2024Review
- Shared Inflammatory Pathology of Stroke and COVID-19.International journal of molecular sciences · 2022Review
- Synthesis and Development of a Novel First-in-Class Cofilin Inhibitor for Neuroinflammation in Hemorrhagic Brain Injury.ACS chemical neuroscience · 2022Article
- The neuroprotective effect of dexmedetomidine and its mechanism.Frontiers in pharmacology · 2022Review
- Long non-coding RNA ncRuPAR regulates gastric cancer cell proliferation and apoptosis via phosphoinositide 3-kinase/protein kinase B signaling.International journal of medical sciences · 2022Article
- Protease-Activated Receptor-1 Antagonist Protects Against Lung Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2021Article
- Research Progress on Alzheimer's Disease and Resveratrol.Neurochemical research · 2020Review
- Thrombin contributes to the injury development and neurological deficit after acute subdural hemorrhage in rats only in collaboration with additional blood-derived factors.BMC neuroscience · 2018Article
- Autophagy in Traumatic Brain Injury: A New Target for Therapeutic Intervention.Frontiers in molecular neuroscience · 2018Review
- Changes in Neuronal Signaling and Cell Stress Response Pathways are Associated with a Multigenic Response of Drosophila melanogaster to DDT Selection.Genome biology and evolution · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Excessive microglial cells activation in response to inflammatory stimuli leads to synaptic loss, dysfunction, and neuronal cell death. Activated microglia are involved in the pathogenesis of neurological conditions and frequently contribute to several complications. Accumulating evidence suggests that signaling through PAR-1 is involved in inflammation, however, its function has yet to be fully elucidated. Here, we have demonstrated that the suppression of PAR-1 leads to down-regulation of inflammatory factors including IL-1β, IL-6, TNF-α, NO, as well as the prevention of activation of NF-κB in BV2 cells. In addition, we found that a PAR-1 antagonist, SCH, prevented LPS-induced excessive microglial activation in a dose-dependent manner. As a result of SCH treatment, neuronal cell death via up-regulation of Akt-mediated pathways was reduced. Our results demonstrate that the beneficial effects of SCH are linked to its ability to block an inflammatory response. Further, we found that SCH inhibited the death of PC12 neurons from the cytotoxicity of activated BV2 cells via activation of the PI3K/Akt pathway. These neuro-protective effects appear to be related to inhibition of PAR-1, and represents a novel neuroprotective strategy that could has potential for use in therapeutic interventions of neuroinflammatory disease.
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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.