ArticleScientific reports2023
Myricetin suppresses traumatic brain injury-induced inflammatory response via EGFR/AKT/STAT pathway.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Nitric oxide and traumatic brain injury.Medical gas research · 2027Review
- Anti-inflammatory phytochemicals from medicinal herbs based on senoinflammation schema for healthy aging.Archives of pharmacal research · 2026Review
- ErbB signaling in brain injury regeneration: Pathway interactions and therapeutic potential.Neural regeneration research · 2026Article
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Exploring potential targets and molecular mechanisms of traumatic brain injury exacerbated by Benzo(a)pyrene via network toxicology and molecular dynamics simulation.Cell biology and toxicology · 2025Article
- Myricetin Attenuates IMQ-Induced Psoriatic Inflammation Through Multi-Target Modulation: Evidence from Network Pharmacology and Experimental Validation.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Myricetin Suppresses Inflammatory Th17 Polarization to Mitigate Alzheimer's Disease Pathogenesis.CNS neuroscience & therapeutics · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- miR-484 in Hippocampal Astrocytes of Aged and Young Rats Targets CSF-1 to Regulate Neural Progenitor/Stem Cell Proliferation and Differentiation Into Neurons.CNS neuroscience & therapeutics · 2025Article
- The Potential of Selected Plants and Their Biologically Active Molecules in the Treatment of Depression and Anxiety Disorders.International journal of molecular sciences · 2025Review
- Exploring the Neuroprotective Potentials of Flavonoid Metabolites inJournal of experimental pharmacology · 2025Review
- Natural products for intervertebral disc degeneration: mechanistic insights and therapeutic potentials.Frontiers in pharmacology · 2025Review
- Astrocyte-derived Interleukin-31 causes poor prognosis in elderly patients with intracerebral hemorrhage.Brain pathology (Zurich, Switzerland) · 2024Article
- Modulation of the LIMK Pathway by Myricetin: A Protective Strategy Against Neurological Impairments in Spinal Cord Injury.Neurospine · 2024Article
- CD300LFCNS neuroscience & therapeutics · 2024Article
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a common disease in neurosurgery with a high fatality and disability rate which imposes a huge burden on society and patient's family. Inhibition of neuroinflammation caused by microglia activation is a reasonable strategy to promote neurological recovery after TBI. Myricetin is a natural flavonoid that has shown good therapeutic effects in a variety of neurological disease models, but its therapeutic effect on TBI is not clear. We demonstrated that intraperitoneal injection of appropriate doses of myricetin significantly improved recovery of neurological function after TBI in Sprague Dawley rats and inhibited excessive inflammatory responses around the lesion site. Myricetin dramatically reduced the expression of toxic microglia markers generated by TBI and LPS, according to the outcomes of in vivo and in vitro tests. In particular, the expression of inducible nitric oxide synthase, cyclooxygenase 2, and some pro-inflammatory cytokines was reduced, which protected learning and memory functions in TBI rats. Through network pharmacological analysis, we found that myricetin may inhibit microglia hyperactivation through the EGFR-AKT/STAT pathway. These findings imply that myricetin is a promising treatment option for the management of neuroinflammation following TBI.
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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.