ArticleNeurotoxicity research2020
Knockdown of TLR4 Represses the Paraquat-Induced Neuroinflammation and Microglial M1 Polarization.
Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Bacillus cereus Induces Necroptosis in Microglia via the RIPK1/3-MLKL Pathway.MicrobiologyOpen · 2026Article
- Synergistic effects of lipopolysaccharide and rotenone on dopamine neuronal damage in rats.CNS neuroscience & therapeutics · 2023Article
- Integrin Mac1 mediates paraquat and maneb-induced learning and memory impairments in mice through NADPH oxidase-NLRP3 inflammasome axis-dependent microglial activation.Journal of neuroinflammation · 2023Article
- Enhanced IRE1α Phosphorylation/Oligomerization-Triggered XBP1 Splicing Contributes to Parkin-Mediated Prevention of SH-SY5Y Cell Death under Nitrosative Stress.International journal of molecular sciences · 2023Article
- The role of Toll-like receptors and neuroinflammation in Parkinson's disease.Journal of neuroinflammation · 2022Review
- MiR-124 Prevents the Microglial Proinflammatory Response by Inhibiting the Activities of TLR4 and Downstream NLRP3 in Palmitic Acid-Treated BV2 Cells.Journal of molecular neuroscience : MN · 2022Article
- Baicalein-A Potent Pro-Homeostatic Regulator of Microglia in Retinal Ischemic Injury.Frontiers in immunology · 2022Article
- The Promise of the Zebrafish Model for Parkinson's Disease: Today's Science and Tomorrow's Treatment.Frontiers in genetics · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Paraquat (PQ) is associated with multiple nervous system disorders including Parkinson's disease. Despite the evidence that PQ could induce inflammatory responses in the central nervous system and largely contribute to neurotoxicity, the mechanisms of PQ-induced neuroinflammation are not yet fully understood. Toll-like receptor 4 (TLR4) could recognize various pathogens and initiate inflammation processes. Therefore, we investigated the role of TLR4 in PQ-induced neuroinflammation by using murine microglial immortalized BV-2 cell line. Normal microglia and TLR4-knockdown microglia were treated with PQ to evaluate signal transduction molecular expression, inflammatory responses, and microglial functions. Compared with normal microglia, PQ-induced production of pro-inflammatory cytokines was significantly reduced in TLR4-knockdown microglia. Levels of M1 markers were decreased, while levels of M2 markers were increased upon PQ exposure, confirming that TLR4 depletion inhibited the microglial M1 polarization. Besides, the migration and phagocytosis capability reduced by PQ were to some extent recovered in TLR4-knockdown microglia. Taken together, our results suggested that TLR4 mediated the neuroinflammatory responses in microglia and the depletion of TLR4 protects against PQ neurotoxicity.
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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.