ArticleInternational journal of molecular sciences2017
Licochalcone A Prevents the Loss of Dopaminergic Neurons by Inhibiting Microglial Activation in Lipopolysaccharide (LPS)-Induced Parkinson's Disease Models.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 83 citations in OpenAlex.
- Peripheral immunochemical considerations in Parkinson disease: sources, targets and crosstalk mechanisms.Journal of translational medicine · 2026Review
- Detection and pharmacokinetics of licochalcone A in brains of neuroinflammatory mouse model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- From Demyelination to Intervention: Natural Compounds as Emerging Therapeutic Targets in Multiple Sclerosis Neuroinflammation.Journal of immunology research · 2026Review
- The geroprotective potential of chalcones.Nature communications · 2025Review
- Recent Advances in the Synthesis and Biological Applications of Prenylated Chalcones.International journal of molecular sciences · 2025Review
- Licochalcone A prevents cognitive decline in a lipopolysaccharide-induced neuroinflammation mice model.Molecular medicine (Cambridge, Mass.) · 2025Article
- Enhancing autophagy mitigates LPS-induced neuroinflammation by inhibiting microglial M1 polarization and neuronophagocytosis.Frontiers in cellular neuroscience · 2025Article
- Research Advances in the Efficacy and Mechanism of Guipi Capsule in Reducing Insomnia.International journal of general medicine · 2025Review
- Crosstalk between neuroinflammation and ferroptosis: Implications for Parkinson's disease progression.Frontiers in pharmacology · 2025Review
- Neuroprotective potential of isofraxidin: Alleviating parkinsonian symptoms, inflammation and microglial activation.Journal of central nervous system disease · 2025Article
- Impact on Human Health ofInternational journal of molecular sciences · 2024Review
- Exploring the neuroprotective potential of Nrf2-pathway activators against annonacin toxicity.Scientific reports · 2024Article
- Article
- Licochalcone A: a review of its pharmacology activities and molecular mechanisms.Frontiers in pharmacology · 2024Review
- Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway.Redox report : communications in free radical research · 2023Article
- Licochalcone A: A Potential Multitarget Drug for Alzheimer's Disease Treatment.International journal of molecular sciences · 2023Review
- Licochalcone A Inhibits Prostaglandin EMolecules (Basel, Switzerland) · 2023Article
- Effects of Herbs and Derived Natural Products on Lipopolysaccharide-Induced Toxicity: A Literature Review.Oxidative medicine and cellular longevity · 2023Review
- Licochalcone B, a Natural Autophagic Agent for Alleviating Oxidative Stress-Induced Cell Death in Neuronal Cells andPharmaceuticals (Basel, Switzerland) · 2022Article
- Natural Products as Novel Neuroprotective Agents; Computational Predictions of the Molecular Targets, ADME Properties, and Safety Profile.Plants (Basel, Switzerland) · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuroprotective effects of Licochalcone A (Lico.A), a flavonoid isolated from the herb licorice, in Parkinson's disease (PD) have not been elucidated. The prominent pathological feature of PD is the loss of dopaminergic neurons. The crucial role of neuroinflammation induced by activated microglia in dopaminergic neurodegeneration has been validated. In this study, we explore the therapeutic effects of Lico.A in lipopolysaccharide (LPS)-induced PD models in vivo and in vitro. We find that Lico.A significantly inhibits LPS-stimulated production of pro-inflammatory mediators and microglial activation by blocking the phosphorylation of extracellular signal-regulated kinase (ERK1/2) and nuclear factor κB (NF-κB) p65 in BV-2 cells. In addition, through cultured primary mesencephalic neuron-glia cell experiments, we illustrate that Lico.A attenuates the decrease in [³H] dopamine (DA) uptake and the loss of tyrosine hydroxylase-immunoreactive (TH-ir) neurons in LPS-induced PD models in vitro. Furthermore, LPS intoxication in rats results in microglial activation, dopaminergic neurodegeneration and significant behavioral deficits in vivo. Lico.A treatment prevents microglial activation and reduction of dopaminergic neuron and ameliorates PD-like behavioral impairments. Thus, these results demonstrate for the first time that the neuroprotective effects of Lico.A are associated with microglia and anti-inflammatory effects in PD models.
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