ArticleNeurotoxicity research2021
Liquiritigenin Decreases Aβ Levels and Ameliorates Cognitive Decline by Regulating Microglia M1/M2 Transformation in AD Mice.
Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Oxidative stress biomarkers and flavonoids in Alzheimer's disease: current clinical evidence and therapeutic perspectives.Redox report : communications in free radical research · 2026Review
- Regulation of NLRP3 inflammasome signaling in Alzheimer's disease: emerging neuroprotective role of phytochemicals.Inflammopharmacology · 2026Review
- Phytochemicals from Brazilian Red Propolis: A Review of Their Anti-Inflammatory Potential.Plants (Basel, Switzerland) · 2025Review
- Natural Products in the Treatment of Neuroinflammation at Microglia: Recent Trend and Features.Cells · 2025Review
- Neuroactive Phytoconstituents ofCurrent topics in medicinal chemistry · 2025Review
- The changes of NLRs family members in the brain of AD mouse model and AD patients.Frontiers in immunology · 2025Article
- Diosmin ameliorates inflammation, apoptosis and activates PI3K/AKT pathway in Alzheimer's disease rats.Metabolic brain disease · 2024Article
- Research progress of natural products and their derivatives against Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2023Review
- Liquiritigenin promotes osteogenic differentiation and prevents bone loss via inducing auto-lysosomal degradation and inhibiting apoptosis.Genes & diseases · 2023Article
- Aerobic exercise reverses the NF-κB/NLRP3 inflammasome/5-HT pathway by upregulating irisin to alleviate post-stroke depression.Annals of translational medicine · 2022Article
- Ginkgolide B inactivates the NLRP3 inflammasome by promoting autophagic degradation to improve learning and memory impairment in Alzheimer's disease.Metabolic brain disease · 2022Article
- Medicine-Food Herbs against Alzheimer's Disease: A Review of Their Traditional Functional Features, Substance Basis, Clinical Practices and Mechanisms of Action.Molecules (Basel, Switzerland) · 2022Review
- Review
- The Role of NLRP3 Inflammasome in Alzheimer's Disease and Potential Therapeutic Targets.Frontiers in pharmacology · 2022Review
- Beneficial effects of natural flavonoids on neuroinflammation.Frontiers in immunology · 2022Review
- A novel strategy for bioactive natural products targeting NLRP3 inflammasome in Alzheimer's disease.Frontiers in pharmacology · 2022Review
- Article
- Shaoyao-Gancao Decoction Promoted Microglia M2 Polarization via the IL-13-Mediated JAK2/STAT6 Pathway to Alleviate Cerebral Ischemia-Reperfusion Injury.Mediators of inflammation · 2022Article
- A network pharmacology study with molecular docking to investigate the possibility of licorice against posttraumatic stress disorder.Metabolic brain disease · 2021Article
- Plant-Derived Compounds as Promising Therapeutics for Vitiligo.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is one of the most common neurodegenerative diseases and is currently incurable. Amyloid β protein (Aβ) deposition is the main pathogenesis of AD, and many studies have shown that Aβ accumulation is toxic to neurons, leading to the inflammatory reaction, neuronal apoptosis, and neurofibrillary tangles. Thus, reducing Aβ levels might be a potential therapeutic strategy for AD. Liquiritigenin (LG), a dihydroflavone monomer compound extracted from natural plant licorice, has a variety of biological activities such as antioxidant, anti-tumor, anti-inflammatory and anti-virus. However, the exact function of LG in the pathogenesis of AD is elusive. Here, we reported that LG could significantly attenuate neuronal apoptosis in Aβ-induced N2A cells and APP/PS1 transgenic mice. Our in vivo and in vitro studies revealed that LG could alleviate the inflammation response, reflected by the reduction of NLRP3 and cleaved caspase-1. Meanwhile, we also found that LG was able to shift M1 type microglia towards M2 type microglia in Aβ-induced BV2 cells and AD mice. Furthermore, LG could reduce the Aβ levels by decreasing APP processing and accelerating Aβ clearance in AD mice. More importantly, daily treatment of LG (30 mg/kg day) for 90 days dramatically ameliorated the spatial learning and memory of AD mice. Taken together, these results suggest that LG can reduce the Aβ levels by regulating the M1/M2 transformation of microglia, thereby reversing memory decline during AD development, suggesting that LG may be a potential therapeutic agent for treating AD.
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