没食子酸通过调节 NF-κB、TNF-α 和 Caspase 3 基因的表达,减轻氧化应激和大鼠海马神经元的损失,从而改善 LPS 引起的记忆力衰退。

IF 3.2 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Maryam Dastan, Ziba Rajaei, Mohammadreza Sharifi, Hossein Salehi
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引用次数: 0

摘要

神经炎症和细胞凋亡在阿尔茨海默病(AD)的发病机制中起着至关重要的作用,而阿尔茨海默病是大多数老年痴呆症的罪魁祸首。没食子酸是一种酚类化合物,具有清除自由基、抗炎和抗细胞凋亡的活性。本研究旨在探讨没食子酸对 LPS 诱导的空间记忆损伤的保护作用及其内在机制。雄性 Wistar 大鼠口服没食子酸(100 毫克/千克)12 天。第8-12天腹腔注射1毫克/千克剂量的LPS。采用莫里斯水迷宫范式评估大鼠的空间学习和记忆能力。评估了大鼠海马中核因子卡巴B(NF-κB)、肿瘤坏死因子-α(TNF-α)和Caspase 3的mRNA水平、脂质过氧化和总硫醇水平。此外,还评估了大脑中神经元的损失和组织学变化。LPS 处理导致空间学习和记忆损伤,NF-κB、TNF-α 和 Caspase 3 mRNA 表达上调,脂质过氧化增加,总硫醇水平下降,海马神经元丢失。此外,100 毫克/公斤剂量的没食子酸可改善记忆力衰退,降低 NF-κB、TNF-α 和 Caspase 3 的 mRNA 水平,减少脂质过氧化,增加海马中总硫醇水平。没食子酸还能防止 LPS 诱导的神经元损失和大脑组织学变化。总之,我们的研究表明,没食子酸对 LPS 诱导的大鼠记忆力衰退具有神经保护作用。这一结果可能与没食子酸的抗炎、抗氧化和抗细胞凋亡活性有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gallic acid ameliorates LPS-induced memory decline by modulating NF-κB, TNF-α, and Caspase 3 gene expression and attenuating oxidative stress and neuronal loss in the rat hippocampus.

Neuroinflammation and apoptosis play critical roles in the pathogenesis of Alzheimer's disease (AD), which is responsible for most cases of dementia in the elderly people. Gallic acid is a phenolic compound with radical scavenging, anti-inflammatory and anti-apoptotic activities. This study aimed to explore the protective effects of gallic acid on LPS-induced spatial memory impairment and find the underlying mechanisms. Gallic acid was orally administered (100 mg/kg) to male Wistar rats for 12 days. LPS was injected intraperitoneally at a dose of 1 mg/kg on days 8-12. Morris water maze paradigm was used to evaluate spatial learning and memory. The mRNA level of nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α) and Caspase 3, lipid peroxidation and total thiol level was assessed in the rat hippocampus. Neuronal loss and histological changes were also evaluated in the brain. LPS treatment resulted in spatial learning and memory impairment, upregulation of NF-κB, TNF-α, and Caspase 3 mRNA expression, increased lipid peroxidation, decreased total thiol level, and neuronal loss in the hippocampus. Moreover, treatment with gallic acid at a dosage of 100 mg/kg ameliorated memory decline, reduced the mRNA level of NF-κB, TNF-α, and Caspase 3, decreased lipid peroxidation and increased total thiol level in the hippocampus. Gallic acid also prevented LPS-induced neuronal loss and histological changes in the brain. Conclusively, our study demonstrated that gallic acid exerts neuroprotective effect against LPS-induced memory decline in rats. This outcome could be due to anti-inflammatory, antioxidant, and anti-apoptotic activities of gallic acid.

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来源期刊
Metabolic brain disease
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.
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