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

  • Neuropharmacology. 2025 Feb 1:263:110215. doi: 10.1016/j.neuropharm.2024.110215.
Yan-Dong Ma  1 ,  Hang Liu  1 ,  Qian Chen  1 ,  Yi Zheng  2 ,  Chao-Ren Yan  1 ,  Yan-Song Li  1 ,  Yi-Xuan Wang  1 ,  Yu-Ting Dai  1 ,  Yang-Hua Jiang  3 ,  Jing-Ming Shi  4
Affiliations
  • 1. Key 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.
  • 2. School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
  • 3. Laboratory Medical Center of the First People's Hospital of Chenzhou City, Chenzhou, Hunan province, 423000, China. Electronic address: [email protected].
  • 4. Key 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. Electronic address: [email protected].
PMID: 39536861 DOI: 10.1016/j.neuropharm.2024.110215
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.

Keywords
Gallic acid; Loganic acid; NF-КB signaling pathway; Neuroinflammation; Primary microglia.
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