Neuroinflammation is a predisposing factor for the development of cognitive impairment and dementia. Among the new molecules that are currently being studied, ellagic acid (EA) has stood out for its neuroprotective properties. The present study investigated the effects of ellagic acid in the object recognition test, oxidative stress, cholinergic neurotransmission, glial cell expression, and phosphorylated Tau protein expression. For this, 32 male Wistar rats received an intraperitoneal (IP) application of lipopolysaccharides (LPS) at a dose of 250 µg/kg or 0.9% saline solution (SAL) for 8 days. Two hours after the IP injections, the animals received 100 mg/kg of EA or SAL via intragastric gavage. Behavioral parameters (open field test and object recognition) were performed on days 5, 6, and 7 of the experimental periods. The results showed that the treatment with EA in the LPS group was able to inhibit cognitive impairment, modulate the immune system response by significantly reducing glial cell expression, attenuating phosphorylated Tau and oxidative damage with consequent improvement in the antioxidant system, as well as preventing the increase of acetylcholinesterase activity. Thus, the neuroprotective effects of EA and its therapeutic potential in cognitive disorders secondary to neuroinflammation were demonstrated.

神经炎症是认知障碍和痴呆症发展的诱因。在目前正在研究的新分子中，鞣花酸（EA）因其神经保护特性而脱颖而出。本研究调查了鞣花酸在对象识别测试，氧化应激，胆碱能神经传递，神经胶质细胞表达和磷酸化Tau蛋白表达中的作用。为此，对32只雄性Wistar大鼠以250 µg / kg的剂量或0.9％的盐溶液（SAL）腹膜内（IP）施用脂多糖（LPS），持续8天。腹膜内注射后两个小时，动物通过胃管饲喂接受100 mg / kg EA或SAL。在实验期的第5、6和7天执行行为参数（开放式测试和物体识别）。结果表明，LPS组中的EA治疗能够抑制认知障碍，通过显着降低神经胶质细胞表达，减弱磷酸化Tau和氧化损伤来调节免疫系统反应，从而改善抗氧化系统，并预防增加乙酰胆碱酯酶活性。因此，证明了EA对继发于神经炎症的认知障碍的神经保护作用及其治疗潜力。