Exploring the molecular mechanisms underlying neuroprotective effect of ellagic acid in okadaic acid-induced Alzheimer's phenotype.

IF 3.2 3区医学 Q2 ENDOCRINOLOGY & METABOLISM Metabolic brain disease Pub Date : 2024-08-12 DOI:10.1007/s11011-024-01405-9

Tourandokht Baluchnejadmojarad, Mehrdad Roghani

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Abstract

Pomegranate polyphenol ellagic acid has medicinal potential in neurodegenerative disorders. The advantageous effect of this polyphenol in improving cognition in okadaic acid (OA)-instigated murine model with unraveling some modes of its action was assessed. Rats received ICV okadaic acid (OA) and post-treated with oral ellagic acid for 3 weeks (25 and 100 mg/kg/day). Cognition was analyzed in behavioral tasks besides assessment of oxidative, apoptotic, and inflammatory factors in addition to hippocampal histochemical analysis. Ellagic acid at a dose of 100 mg/kg properly attenuated cognitive abnormalities in novel object recognition (NOR), Y maze, and Barnes maze tests. Additionally, ellagic acid diminished hippocampal changes of malondialdehyde (MDA), protein carbonyl, reactive oxygen species (ROS), glutathione (GSH), glutathione peroxidase, superoxide dismutase (SOD), apoptotic factors caspases 1 and 3, tumor necrosis factor α (TNFα), and acetylcholinesterase (AChE) and beta secretase 1 (BACE 1) besides reversal of AMP-activated protein kinase (AMPK) and hyperphosphorylated tau (p-tau). Moreover, lower glial fibrillary acidic protein (GFAP) and less injury of hippocampal CA1 pyramidal neurons were observed upon ellagic acid. To conclude, neuroprotective potential of ellagic acid was shown which is somewhat attributable to its reversal of oxidative, apoptotic, and neuroinflammatory events in addition to proper regulation of AMPK and p-tau.

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探索鞣花酸在 okadaic 酸诱导的阿尔茨海默氏症表型中发挥神经保护作用的分子机制。

石榴多酚鞣花酸具有治疗神经退行性疾病的潜力。本研究评估了石榴多酚在改善冈田酸（OA）诱导的小鼠模型中的认知能力方面的优势作用，并揭示了其某些作用模式。大鼠接受 ICV 秋田酸（OA）治疗后，口服鞣花酸 3 周（25 和 100 毫克/千克/天）。除了评估氧化、凋亡和炎症因子以及海马组织化学分析外，还对行为任务中的认知能力进行了分析。剂量为100毫克/千克的鞣花酸可适当减轻新物体识别（NOR）、Y迷宫和巴恩斯迷宫测试中的认知异常。此外，鞣花酸还能减少海马中丙二醛（MDA）、蛋白质羰基、活性氧（ROS）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶、超氧化物歧化酶（SOD）的变化、除了逆转 AMP 激活蛋白激酶（AMPK）和高磷酸化 tau（p-tau）外，还能抑制凋亡因子 caspases 1 和 3、肿瘤坏死因子 α（TNFα）、乙酰胆碱酯酶（AChE）和 beta 分泌酶 1（BACE 1）。此外，鞣花酸还能降低胶质纤维酸性蛋白（GFAP），减少对海马 CA1 锥体神经元的损伤。总之，鞣花酸具有神经保护潜力，这在一定程度上可归因于它除了能适当调节 AMPK 和 p-tau 外，还能逆转氧化、凋亡和神经炎症事件。

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来源期刊

Metabolic brain disease 医学-内分泌学与代谢

CiteScore

5.90

自引率

5.60%

发文量

248

审稿时长

6-12 weeks

期刊介绍： Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.