ArticleCellular and molecular neurobiology2018
Toll-Like Receptor 4 Knockdown Attenuates Brain Damage and Neuroinflammation After Traumatic Brain Injury via Inhibiting Neuronal Autophagy and Astrocyte Activation.
Article in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Adolescent Ethanol Exposure Disrupts the Mature Phenotype of Surviving Neuroprogenitors in Female Mice.Hippocampus · 2026Article
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- Research Progress on Spinal Cord Repair Based on Regulation of the Neuroregenerative Microenvironment.Cellular and molecular neurobiology · 2026Review
- Research Progress on Regulating Autophagy in Traditional Chinese Medicine for the Treatment of Traumatic Brain Injury.ACS omega · 2025Review
- A comprehensive literature review on the effects of saffron and its bioactive components on traumatic brain injury (TBI).Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- TLR4 Targeting: A Promising Therapeutic Approach Across Multiple Human Diseases.Current protein & peptide science · 2025Review
- Administration of monophosphoryl lipid A shortly after traumatic brain injury blocks the following spatial and avoidance memory loss and neuroinflammation.Scientific reports · 2024Article
- Neuron-specific deficiency of autophagy increases neuronal loss in traumatic brain injury.PNAS nexus · 2024Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- The contribution of the meningeal immune interface to neuroinflammation in traumatic brain injury.Journal of neuroinflammation · 2024Review
- Autophagy in Neuroinflammation: A Focus on Epigenetic Regulation.Aging and disease · 2024Review
- Treatment with Rapamycin in Animal Models of Traumatic Brain Injuries; a Systematic Review and Meta-Analysis.Archives of academic emergency medicine · 2024Review
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Astrocyte-targeted siRNA delivery by adenosine-functionalized LNP in mouse TBI model.Molecular therapy. Nucleic acids · 2023Article
- Complement C3 Enhances LPS-Elicited Neuroinflammation and Neurodegeneration Via the Mac1/NOX2 Pathway.Molecular neurobiology · 2023Article
- Exosomes and Nano-SDF Scaffold as a Cell-Free-Based Treatment Strategy Improve Traumatic Brain Injury Mechanisms by Decreasing Oxidative Stress, Neuroinflammation, and Increasing Neurogenesis.Stem cell reviews and reports · 2023Article
- TLR4 Enhances Cerebral Ischemia/Reperfusion Injury via Regulating NLRP3 Inflammasome and Autophagy.Mediators of inflammation · 2023Article
- Hydroxychloroquine attenuates neuroinflammation following traumatic brain injury by regulating the TLR4/NF-κB signaling pathway.Journal of neuroinflammation · 2022Article
- Ouabain-NaNeurochemical research · 2022Article
- Specific microRNAs for Modulation of Autophagy in Spinal Cord Injury.Brain sciences · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 4 (TLR4) has been linked to various pathophysiological conditions, such as traumatic brain injury (TBI). It is reported that posttraumatic neuroinflammation is an essential event in the progression of brain injury after TBI. Recent evidences indicate that TLR4 mediates glial phagocytic activity and inflammatory cytokines production. Thus, TLR4 may be an important therapeutic target for neuroinflammatory injury post-TBI. This study was designed to explore potential effects and underlying mechanisms of TLR4 in rats suffered from TBI. TBI model was induced using a controlled cortical impact in rats, and application of TLR4 shRNA silenced TLR4 expression in brain prior to TBI induction. Elevated TLR4 was specifically observed in the hippocampal astrocytes and neurons posttrauma. Interestingly, TLR4 shRNA decreased the concentrations of interleukin (IL)-1β, IL-6, and tissue necrosis factor-α; alleviated hippocampal neuronal damage; reduced brain edema formation; and improved neurological deficits after TBI. Meanwhile, to further explore underlying molecular mechanisms of this neuroprotective effects of TLR4 knockdown, our results showed that TLR4 knockdown significantly inhibited the upregulation of autophagy-associated proteins caused by TBI. More importantly, an autophagy inducer, rapamycin pretreated, could partially abolish neuroprotective effects of TLR4 knockdown on TBI rats. Furthermore, TLR4 silencing markedly suppressed GFAP upregulation and improved cell hypertrophy to attenuate TBI-induced astrocyte activation. Taken together, these findings suggested that TLR4 knockdown ameliorated neuroinflammatory response and brain injury after TBI through suppressing autophagy induction and astrocyte activation.
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