本研究通过应用一种抗氧化剂——α-糖基异槲皮苷（AGIQ），研究脂多糖（LPS）诱导的大鼠认知功能障碍模型中，神经炎症的作用。实验中，6周龄的大鼠在饮食中添加0.5%（w/w）AGIQ，持续38天，并在第8和第10天每天一次腹腔注射1mg/kg体重的LPS。第11天，单独使用LPS在海马和大脑皮层中增加或有增加白细胞介素-1β和肿瘤坏死因子-α。免疫组化结果表明，单独使用LPS增加了齿状回髂部（DG）的Iba1 +和CD68 +小胶质细胞和GFAP +星形胶质细胞的数量。AGIQ处理降低或有降低脑部炎症性细胞因子水平和DG髂部中CD68 +小胶质细胞数。在第34和第38天的情境恐惧条件反射试验中，单独使用LPS会损害恐惧记忆的获得，而AGIQ则有助于恢复这种障碍。在第38天，单独使用LPS会减少神经发生区的DCX +细胞数量，而AGIQ则增加了颗粒层下颗粒前神经前体细胞+（PCNA +）细胞和CALB2 +髂间神经元的数量。此外，单独使用LPS会减少或有减少突触可塑性相关的FOS +和COX2 +颗粒细胞数量，而AGIQ则恢复了它们。结果表明，LPS处理诱导急性神经炎症，随后引起新生颗粒细胞神经发生无序，进而导致恐惧记忆获得障碍。相反，AGIQ具有抗炎作用，改善LPS引起的不良影响。这些结果表明，神经炎症是LPS引起恐惧记忆获得障碍的关键因素。

This study investigated the role of neuroinflammation in a lipopolysaccharides (LPS)-induced cognitive dysfunction model in rats using an antioxidant, α-glycosyl isoquercitrin (AGIQ). Six-week-old rats were dietary treated with 0.5% (w/w) AGIQ for 38 days, and LPS at 1 mg/kg body weight was administered intraperitoneally once daily on Days 8 and 10. On Day 11, LPS alone increased or tended to increase interleukin-1β and tumor necrosis factor-α in the hippocampus and cerebral cortex. Immunohistochemically, LPS alone increased the number of Iba1+ and CD68+ microglia, and GFAP+ astrocytes in the hilus of the hippocampal dentate gyrus (DG). AGIQ treatment decreased or tended to decrease brain proinflammatory cytokine levels and the number of CD68+ microglia in the DG hilus. In the contextual fear conditioning test during Day 34 and Day 38, LPS alone impaired fear memory acquisition, and AGIQ tended to recover this impairment. On Day 38, LPS alone decreased the number of DCX+ cells in the neurogenic niche, and AGIQ increased the numbers of PCNA+ cells in the subgranular zone and CALB2+ hilar interneurons. Additionally, LPS alone decreased or tended to decrease the number of synaptic plasticity-related FOS+ and COX2+ granule cells and AGIQ recovered them. The results suggest that LPS administration induced acute neuroinflammation and subsequent impairment of fear memory acquisition caused by suppressed synaptic plasticity of newborn granule cells following disruptive neurogenesis. In contrast, AGIQ exhibited anti-inflammatory effects and ameliorated LPS-induced adverse effects. These results suggest that neuroinflammation is a key factor in the development of LPS-induced impairment of fear memory acquisition.