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鞣花酸抑制脂多糖诱导的神经炎症和认知障碍。

Ellagic Acid Inhibits Neuroinflammation and Cognitive Impairment Induced by Lipopolysaccharides.

机构信息

Departamento de Clínica de Pequenos Animais, Universidade Federal de Santa Maria, Av. Roraima 1000, Santa Maria, RS, 97105-900, Brazil.

Departamento de Bioquímica, Universidade Federal de Santa Maria, Av. Roraima, 1000, Santa Maria, RS, 97105-900, Brazil.

出版信息

Neurochem Res. 2020 Oct;45(10):2456-2473. doi: 10.1007/s11064-020-03105-z. Epub 2020 Aug 10.

DOI:10.1007/s11064-020-03105-z
PMID:32779097
Abstract

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.

摘要

神经炎症是认知障碍和痴呆发展的一个促成因素。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物体识别测试、氧化应激、胆碱能神经递质、神经胶质细胞表达和磷酸化 Tau 蛋白表达中的作用。为此,32 只雄性 Wistar 大鼠接受了腹腔内 (IP) 注射 250µg/kg 的脂多糖 (LPS) 或 0.9%生理盐水 (SAL) 8 天。在 IP 注射后 2 小时,动物通过灌胃接受 100mg/kg 的 EA 或 SAL。在实验期的第 5、6 和 7 天进行行为参数(旷场试验和物体识别)。结果表明,EA 在 LPS 组的治疗能够抑制认知障碍,通过显著降低神经胶质细胞表达来调节免疫系统反应,减轻磷酸化 Tau 和氧化损伤,从而改善抗氧化系统,并防止乙酰胆碱酯酶活性的增加。因此,证明了 EA 的神经保护作用及其在神经炎症引起的认知障碍中的治疗潜力。

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