Lithocarpus polystachyus Rehd. leaves aqueous extract inhibits learning and memory impairment in Alzheimer's disease rats: Involvement of the SIRT6/NLRP3 signaling pathway

Ibrain Pub Date : 2024-06-03 DOI:10.1002/ibra.12164
Wendan Wu, You Yan, Tingting Yi, Yu Wei, Jian-mei Gao, Qihai Gong
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Abstract

Alzheimer's disease (AD) is a chronic and progressive neurodegenerative condition that is influenced by multiple factors along with neuroinflammation and oxidative stress. Our previous study proved that Lithocarpus polystachyus Rehd. aqueous extract (sweet tea aqueous extract, STAE) effectively inhibits hydrogen peroxide‐induced neuronal cell injury. However, it is not clear whether STAE can protect against AD, and its underlying mechanisms are still uncertain. Therefore, the present study was designed to evaluate the possible behavioral and neurochemical effects of STAE on Aβ25‐35‐induced AD rats administered STAE (20, 40, 80 mg/mL) for 14 days. We showed that STAE administration significantly and dose‐dependently ameliorated the cognitive deficits in the AD rat models, assessed in the Morris water maze (MWM) test, Y‐maze test, and novel object recognition (NOR) test. The results of hematoxylin and eosin (H&E) staining and Nissl staining showed that after treatment with STAE, the pathological damage to the hippocampal CA1, CA3, and dentate gyrus (DG) neurons of rats was significantly improved. Furthermore, STAE dose‐dependently inhibited microglia and astrocyte activation in the hippocampus of rats accompanied by increased protein expression of silent mating‐type information regulation 2 homolog 6 (SIRT6) and decreased protein expression of nod‐like receptor thermal protein domain‐associated protein 3 (NLRP3) and its downstream pyroptosis‐related genes after following Aβ25‐35. In summary, our findings indicate that STAE effectively inhibits Aβ25‐35‐induced learning and memory impairment in rats, and the mechanism is, at least partially, related to the regulation of SIRT6/NLRP3 signaling pathway.
石蒜叶水提取物可抑制阿尔茨海默病大鼠的学习和记忆损伤:SIRT6/NLRP3信号通路的参与
阿尔茨海默病(AD)是一种慢性进行性神经退行性疾病,受到神经炎症和氧化应激等多种因素的影响。我们之前的研究证明,甜茶水提取物(Lithocarpus polystachyus Rehd.)能有效抑制过氧化氢诱导的神经细胞损伤。然而,甜茶水提取物是否能预防注意力缺失症尚未明确,其潜在机制也尚不清楚。因此,本研究旨在评估STAE对Aβ25-35诱导的AD大鼠可能产生的行为和神经化学效应。我们的研究表明,在莫里斯水迷宫(MWM)测试、Y-迷宫测试和新物体识别(NOR)测试中,STAE能显著改善AD大鼠模型的认知缺陷,且与剂量相关。苏木精和伊红(H&E)染色及Nissl染色结果表明,STAE治疗后,大鼠海马CA1、CA3和齿状回(DG)神经元的病理损伤明显改善。此外,STAE剂量依赖性地抑制了大鼠海马中小胶质细胞和星形胶质细胞的活化,同时还增加了沉默配子型信息调控2同源物6(SIRT6)的蛋白表达,并降低了Aβ25-35治疗后类结受体热蛋白结构域相关蛋白3(NLRP3)及其下游热变态反应相关基因的蛋白表达。综上所述,我们的研究结果表明,STAE能有效抑制Aβ25-35诱导的大鼠学习和记忆损伤,其机制至少部分与调节SIRT6/NLRP3信号通路有关。
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