ArticleJournal of molecular neuroscience : MN2022
MiR-124 Prevents the Microglial Proinflammatory Response by Inhibiting the Activities of TLR4 and Downstream NLRP3 in Palmitic Acid-Treated BV2 Cells.
Article in Journal of molecular neuroscience : MN, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Diet, Metabolism and Synaptic Function: Integrating Evidence Across Models in Neurodegeneration Research.Biomedicines · 2026Review
- Anti-arthritic efficacy of geraniol and methotrexate via miRNA-driven NLRP3 inflammasome suppression in rat adjuvant-induced arthritis.Inflammopharmacology · 2026Article
- ARG1-polyamine axis: cell-type-specific functions in disease pathogenesis and therapeutic targeting.Frontiers in immunology · 2026Review
- The Role of MicroRNA in the Pathogenesis of Atopic Dermatitis.International journal of molecular sciences · 2025Review
- Role of circ_0012856 in modulating molecular pathways of diabetic peripheral neuropathy.Journal of cell communication and signaling · 2025Article
- High-fat diet and chronic restraint stress exacerbate anxiety-depressive behaviors via astrocytic A1 phenotype transformation.Scientific reports · 2025Article
- Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025Review
- The Yin and Yang of Microglia-Derived Extracellular Vesicles in CNS Injury and Diseases.Cells · 2024Review
- Article
- The role of pyroptosis in cognitive impairment.Frontiers in neuroscience · 2023Review
- Neuroendocrine microRNAs linked to energy homeostasis: future therapeutic potential.Pharmacological reports : PR · 2022Review
- Asiatic Acid Attenuates Inflammation Induced byInternational journal of molecular sciences · 2022Article
- MicroRNA: A Linking between Astrocyte Dysfunction, Mild Cognitive Impairment, and Neurodegenerative Diseases.Life (Basel, Switzerland) · 2022Review
- Cimifugin Ameliorates Lipotoxicity-Induced Hepatocyte Damage and Steatosis through TLR4/p38 MAPK- and SIRT1-Involved Pathways.Oxidative medicine and cellular longevity · 2022Article
- Microglia Pyroptosis: A Candidate Target for Neurological Diseases Treatment.Frontiers in neuroscience · 2022Review
- Regulation by noncoding RNAs of local translation, injury responses, and pain in the peripheral nervous system.Neurobiology of pain (Cambridge, Mass.)Article
- Exploration of the Key Genes Involved in Non-alcoholic Fatty Liver Disease and Possible MicroRNA Therapeutic Targets.Journal of clinical and experimental hepatologyArticle
- Epigenetic regulation in opioid induced hyperalgesia.Neurobiology of pain (Cambridge, Mass.)Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is a mechanism by which obesity or a high-fat diet leads to cognitive impairment. MiR-124, a highly expressed microRNA in the brain, can alleviate neuroinflammation by regulating microglial activation, but its mechanism is unclear. The aim of the study was to explore whether miR-124 exerted this effect through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid-treated BV2 cells. Prepared BV2 cells were treated with palmitic acid to establish an in vitro model of a high-fat diet. An miR-124 mimic and inhibitor were adopted to upregulate and downregulate the expression of miR-124, respectively. TAK-242 and NLRP3 siRNA were used to downregulate the expression of TLR4 and NLRP3. The expression levels of miR-124, signaling proteins (TLR4, MyD88, and NF-κB p65), inflammasome markers (NLRP3 and IL-1β), and microglial activated markers (CD206, Arg-1, CD86, and iNOS) were measured by qPCR and western blotting. The pyroptosis rate was assessed using flow cytometry. First, palmitic acid upregulated TLR4/MyD88/NF-κB p65 signaling, increased NLRP3 expression, elevated the pyroptosis rate, and promoted the microglial proinflammatory response in BV2 cells. Second, the miR-124 mimic and inhibitor separately alleviated and aggravated the effect of palmitic acid on microglial activation and NLRP3 expression. The miR-124 mimic also downregulated TLR4/MyD88/NF-κB p65 signaling. Third, TAK-242 did not affect the expression of miR-124 but simulated the protective effect of the miR-124 mimic on microglial activation and NLRP3 expression. Fourth, NLRP3 siRNA also inhibited the microglial proinflammatory response in BV2 cells. MiR-124 prevented the microglial proinflammatory response through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid-treated BV2 cells.
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