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Updated: Jun 7, 2025
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Gallic acid and loganic acid attenuate amyloid-β oligomer-induced microglia damage via NF-КB signaling pathway
Yan-Dong Ma1, Hang Liu1, Qian Chen1
1Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xian Yang, Shaanxi Province, 712082, China.
Abstract:
Amyloid β peptide (Aβ) induces neurodegeneration in the early stage of Alzheimer's disease (AD), resulting in neuroinflammation, oxidative damage, and mitochondrial impaired function. These reactions were closely associated with the pathological changes of brain microglia. Therefore, it was crucial to investigate the precise process of neuroinflammation induced by Aβ in microglia and discover therapies to alleviate its harmful consequences. This study evaluated the toxicity detection of primary microglia generated by Aβ42 ADDL. identification of inflammatory markers, measurement of ROS, and assessment of mitochondrial energy metabolism, mitochondrial membrane potential damage and mitochondrial ROS to evaluate the reparative properties of natural small molecule compounds Gallic acid and Loganic acid on primary mouse microglia. The findings indicated that Gallic acid and Loganic acid exhibited diverse reparative effects on impaired microglia. Thus, it can be provisionally predicted that Aβ42 ADDL affects microglia and promotes modifications in the NF-кB signaling pathway. Gallic acid and Loganic acid were expected to initially restore the NF-кB signaling pathway, leading to a reduction in M1-microglia and an elevation in M2-microglia, thereby decreasing various inflammatory factors and increasing anti-inflammatory factors. The mitochondrial metabolism, mitochondrial membrane potential, and mitochondrial ROS of primary microglia were restored, leading to a reduction in neuroinflammation.
Insights
Natural compounds Gallic acid and Loganic acid show reparative effects on microglia impaired by amyloid-beta (Aβ) in Alzheimer's disease models. These compounds may reduce neuroinflammation by restoring cellular functions and balancing microglial responses.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Amyloid-beta (Aβ) peptide is a key driver of neurodegeneration in early Alzheimer's disease (AD).
- Aβ-induced neuroinflammation, oxidative damage, and mitochondrial dysfunction are closely linked to microglial pathology.
- Understanding Aβ's precise effects on microglia is crucial for developing effective AD therapies.
Purpose of the Study:
- To evaluate the toxicity of Aβ42 ADDL on primary microglia.
- To assess the reparative properties of Gallic acid and Loganic acid on Aβ-impaired microglia.
- To investigate the impact of these compounds on inflammatory markers, oxidative stress, and mitochondrial function.
Main Methods:
- Primary mouse microglia were exposed to Aβ42 ADDL.
- Toxicity, inflammatory markers, reactive oxygen species (ROS), and mitochondrial parameters (energy metabolism, membrane potential) were measured.
- The effects of Gallic acid and Loganic acid were evaluated on these parameters.
Main Results:
- Aβ42 ADDL induced toxicity and impaired mitochondrial function in primary microglia.
- Gallic acid and Loganic acid demonstrated diverse reparative effects on Aβ-damaged microglia.
- These compounds appeared to restore the NF-κB signaling pathway, shifting microglia from M1 to M2 phenotypes.
Conclusions:
- Gallic acid and Loganic acid show potential in mitigating Aβ-induced microglial dysfunction and neuroinflammation in AD.
- Restoration of the NF-κB pathway and M1/M2 microglial balance is a likely mechanism of action.
- These natural compounds may offer a therapeutic strategy for Alzheimer's disease by reducing neuroinflammation and improving mitochondrial health.
