ArticleFrontiers in immunology2019
Isovitexin-Mediated Regulation of Microglial Polarization in Lipopolysaccharide-Induced Neuroinflammation via Activation of the CaMKKβ/AMPK-PGC-1α Signaling Axis.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
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- Phytochemical and Anti-Ischemic Stroke Properties from theDrug design, development and therapy · 2026Review
- Isovitexin: A Promising Active Compound Found in Nature's Bounty.Plant foods for human nutrition (Dordrecht, Netherlands) · 2025Review
- Xiaoyao San against depression via glia-mediated neuroinflammation using network pharmacology and experimental validation.Scientific reports · 2025Article
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Regulation of lipid dysmetabolism and neuroinflammation progression linked with Alzheimer's disease through modulation of Dgat2.bioRxiv : the preprint server for biology · 2025Article
- Vicenin-2 Hinders Pro-Inflammatory Response via Targeting the CaMKKβ-AMPK-SIRT1 Axis in Lipopolysaccharide-Stressed THP-1 Cells.International journal of molecular sciences · 2025Article
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- Activation of G-protein-coupled receptor 39 reduces neuropathic pain in a rat model.Neural regeneration research · 2024Article
- Apelin-13 Improves Cognitive Impairment and Repairs Hippocampal Neuronal Damage by Activating PGC-1α/PPARγ Signaling.Neurochemical research · 2023Article
- Activation of HCA2 regulates microglial responses to alleviate neurodegeneration in LPS-induced in vivo and in vitro models.Journal of neuroinflammation · 2023Article
- Lipid metabolism and Alzheimer's disease: clinical evidence, mechanistic link and therapeutic promise.The FEBS journal · 2023Review
- Phytochemistry, Pharmacology and Molecular Mechanisms of Herbal Bioactive Compounds for Sickness Behaviour.Metabolites · 2022Review
- Resveratrol Attenuated Manganese-Induced Learning and Memory Impairments in Mice Through PGC-1Alpha-Mediated Autophagy and Microglial M1/M2 Polarization.Neurochemical research · 2022Article
- Puerarin Attenuates Oxidative Stress and Ferroptosis via AMPK/PGC1α/Nrf2 Pathway after Subarachnoid Hemorrhage in Rats.Antioxidants (Basel, Switzerland) · 2022Article
- Anti-Inflammatory Effects of Phytochemical Components ofMolecules (Basel, Switzerland) · 2022Review
- Interleukin-35 exhibits protective effects in a rat model of hypoxic-ischemic encephalopathy through the inhibition of microglia-mediated inflammation.Translational pediatrics · 2022Article
- CB2R Attenuates Intervertebral Disc Degeneration by Delaying Nucleus Pulposus Cell Senescence through AMPK/GSK3β Pathway.Aging and disease · 2022Article
- The Neuroprotection of Verbascoside in Alzheimer's Disease Mediated through Mitigation of Neuroinflammation via Blocking NF-κB-p65 Signaling.Nutrients · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia are the brain's immune cells and play an important role in regulating the microenvironment in the central nervous system. Activated microglia are capable of acquiring the pro-inflammatory (M1) phenotype and anti-inflammatory (M2) phenotype. Overactivation of microglia is neurotoxic and may lead to neuroinflammatory brain disorders. Neuroinflammation in the brain plays a crucial role part in the pathophysiology of many psychiatric and neurological diseases. The inhibition of M1 microglia and promotion of M2 microglia was demonstrated to treat and prevent these diseases through reduced neuroinflammation. Isovitexin (IVX) has anti-inflammatory properties and passes through the blood-brain barrier; however, the molecular mechanism that modulates IVX-mediated microglial polarization remains unclear. In BV-2 cells and mouse primary microglia, IVX suppressed the expression of M1 microglial markers, enhanced the expression of M2 microglial markers, and enhanced the release of interleukin 10 (IL-10). IVX promoted the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and PPARγ coactivator-1α (PGC-1α) in LPS-induced microglial activation. The inhibition of PPARγ and PGC-1α attenuated the regulatory effect of IVX in LPS-induced microglial polarization. IVX increased the expression of p-CaMKKβ, p-AMPK, and PGC-1α in BV-2 cells. Inhibition of CaMKKβ with STO-609 or knockdown of CaMKKβ with CaMKKβ siRNA attenuated IVX-mediated M2 microglial polarization in LPS-treated cells. In LPS-treated mice, the inhibition of CaMKKβ and PGC-1α attenuated the IVX-mediated prevention of sickness behavior and enhanction of IVX-mediated M2 microglial polarization. IVX promoted M2 microglial polarization which exerted anti-inflammatory effects on LPS-induced neuroinflammation via the activation of the CaMKKβ/AMPK-PGC-1α signaling axis.
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