Liquiritigenin Decreases Aβ Levels and Ameliorates Cognitive Decline by Regulating Microglia M1/M2 Transformation in AD Mice
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Yexiang Du1,2, Min Luo1, Yehong Du3
1Department of Anatomy, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing, 400016, People's Republic of China.
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.
Insights
Liquiritigenin (LG) reduces amyloid-beta (Aβ) levels and neuronal apoptosis in Alzheimer's disease (AD) models. This natural compound may offer a therapeutic strategy for AD by modulating microglia and improving memory.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) deposition, neuronal apoptosis, and inflammation.
- Current AD treatments are limited, highlighting the need for novel therapeutic strategies targeting Aβ accumulation and its downstream effects.
- Liquiritigenin (LG), a natural compound from licorice, possesses various biological activities, but its role in AD pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the therapeutic potential of Liquiritigenin (LG) in Alzheimer's disease (AD).
- To elucidate the mechanisms by which LG affects Aβ pathology, neuroinflammation, and cognitive function in AD models.
Main Methods:
- In vitro studies using Aβ-induced N2A cells and BV2 microglia cells.
- In vivo studies using APP/PS1 transgenic mice, a model for Alzheimer's disease.
- Assessment of neuronal apoptosis, inflammatory markers (NLRP3, cleaved caspase-1), microglial polarization (M1/M2), Aβ levels, APP processing, and spatial learning/memory.
Main Results:
- LG significantly attenuated neuronal apoptosis in both cell and animal models of AD.
- LG reduced neuroinflammation by decreasing NLRP3 and cleaved caspase-1 levels and promoting a shift from M1 to M2 microglia.
- LG decreased Aβ levels by reducing APP processing and enhancing Aβ clearance, leading to significant amelioration of spatial learning and memory deficits in AD mice.
Conclusions:
- Liquiritigenin (LG) demonstrates significant therapeutic potential for Alzheimer's disease (AD).
- LG exerts its effects by reducing Aβ levels, alleviating neuroinflammation, and modulating microglial polarization.
- LG may serve as a promising therapeutic agent for AD by reversing cognitive decline associated with the disease.
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