ArticleJournal of neuroinflammation2022
Nilotinib modulates LPS-induced cognitive impairment and neuroinflammatory responses by regulating P38/STAT3 signaling.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- A multistage micro-nano biosystem prevents sepsis-associated encephalopathy through coordinated neuroinflammation suppression and gut-brain axis modulation.Bioactive materials · 2026Article
- The integrated stress response kinase GCN2 prevents ZAKα-Dependent inflammatory hyperactivation in macrophages.The Journal of biological chemistry · 2026Article
- LRP1 Activation Promotes Metabolic Reprogramming and Mrc1 Expression to Attenuate LPS-Induced Cognitive Deficits: An Integrated Omics Analysis.CNS neuroscience & therapeutics · 2026Article
- The insulin receptor inhibitor BMS-754807 alleviates neuroinflammation and Alzheimer's disease pathologies across human cellular and mouse models.Journal of neuroinflammation · 2026Article
- Comparative Evaluation of Imatinib and Nilotinib in a Streptozotocin-Induced Rat Model of Alzheimer's Disease : Neuroprotective, Anti-inflammatory, and Cognitive Outcomes.Journal of Korean Neurosurgical Society · 2026Article
- Entrectinib attenuates LPS-induced neuroinflammation by inhibiting JNK, p38, and AKT pathways and ameliorates cognitive impairment.Archives of pharmacal research · 2026Article
- Beta-lactam Antibiotic Cefepime Attenuates Lipopolysaccharide-induced Pain and Depression By Modulating Inflammatory Response and Astroglial Glutamate Transporter in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- A selective agonist of the prostacyclin receptor alleviates microglial and astroglial neuroinflammatory responses through P38 and NLRP3.Frontiers in immunology · 2026Article
- Spinosin Suppresses RANKL-induced Osteoclastogenesis and Alleviates LPS-induced Cranial Osteolysis: A Study based on Network Pharmacology and Experimental Validation.Current medicinal chemistry · 2026Article
- Non-Catalytic Inhibitors of the p38/MK2 Interface: Repurposing Approved Drugs to Target Neuroinflammation in Alzheimer's Disease.Journal of medicinal chemistry · 2025Article
- Alpha Ketoglutaric Acid attenuates LPS Induced Inflammatory Response by Inhibiting the PKCε/MAPK/P65 Signaling Pathway and Inhibit Oxidative Stress in Kupffer Cells.Inflammation · 2025Article
- Integrated Analysis of Single-Cell and Transcriptome Data Reveals the Role and Regulatory Mechanisms of Neuroinflammation in Parkinson's Disease.Inflammation · 2025Article
- Temporin-GHaR Peptide Alleviates LPS-Induced Cognitive Impairment and Microglial Activation by Modulating Endoplasmic Reticulum Stress.Probiotics and antimicrobial proteins · 2025Article
- Pro-Inflammatory Microglia Exacerbate High-Altitude-Induced Cognitive Impairment by Driving Lipid Droplet Accumulation in Astrocytes.Antioxidants (Basel, Switzerland) · 2025Article
- EZH2 knockout in mice activates STAT3 signalling via STAT3 methylation and modulates ferroptosis in pulpitis-affected dental pulp vascular endothelial cells: A laboratory investigation.International endodontic journal · 2025Article
- Research on the functions and potential mechanisms of STAT3 in chronic myelogenous leukemia.Discover oncology · 2025Article
- Results of the preclinical multicenter randomized controlled paclitaxel-induced neuropathy prevention replication study (PINPRICS).BMC research notes · 2025Article
- Reprogramming Lung Redox Homeostasis by NIR Driven Ultra-Small Pd Loaded Covalent Organic Framework Inhibits NF-κB Pathway for Acute Lung Injury Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Minocycline AmelioratesBrain sciences · 2025Article
- Dual-action kinase inhibitors influence p38α MAP kinase dephosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIn chronic myelogenous leukemia, reciprocal translocation between chromosome 9 and chromosome 22 generates a chimeric protein, Bcr-Abl, that leads to hyperactivity of tyrosine kinase-linked signaling transduction. The therapeutic agent nilotinib inhibits Bcr-Abl/DDR1 and can cross the blood-brain barrier, but its potential impact on neuroinflammatory responses and cognitive function has not been studied in detail.
methodsThe effects of nilotinib in vitro and in vivo were assessed by a combination of RT-PCR, real-time PCR, western blotting, ELISA, immunostaining, and/or subcellular fractionation. In the in vitro experiments, the effects of 200 ng/mL LPS or PBS on BV2 microglial cells, primary microglia or primary astrocytes pre- or post-treated with 5 µM nilotinib or vehicle were evaluated. The in vivo experiments involved wild-type mice administered a 7-day course of daily injections with 20 mg/kg nilotinib (i.p.) or vehicle before injection with 10 mg/kg LPS (i.p.) or PBS.
resultsIn BV2 microglial cells, pre- and post-treatment with nilotinib altered LPS-induced proinflammatory/anti-inflammatory cytokine mRNA levels by suppressing AKT/P38/SOD2 signaling. Nilotinib treatment also significantly downregulated LPS-stimulated proinflammatory cytokine levels in primary microglia and primary astrocytes by altering P38/STAT3 signaling. Experiments in wild-type mice showed that nilotinib administration affected LPS-mediated microglial/astroglial activation in a brain region-specific manner in vivo. In addition, nilotinib significantly reduced proinflammatory cytokine IL-1β, IL-6 and COX-2 levels and P38/STAT3 signaling in the brain in LPS-treated wild-type mice. Importantly, nilotinib treatment rescued LPS-mediated spatial working memory impairment and cortical dendritic spine number in wild-type mice.
conclusionsOur results indicate that nilotinib can modulate neuroinflammatory responses and cognitive function in LPS-stimulated wild-type mice.
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