Gallic acid and loganic acid attenuate amyloid-β oligomer-induced microglia damage via NF-КB signaling pathway.

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.