菝葜皂苷元对高脂饮食诱导认知障碍大鼠的影响
Effects of Smilapogenin on Rats with Cognitive Impairment Induced by High-fat Diet
马锦梦1
作者信息
- 1. 郑州工商学院体育学院,郑州,451400
- 折叠
摘要
本研究旨在探究知母源性菝葜皂苷元对高脂饮食诱导认知障碍大鼠认知功能的影响,并进一步研究其潜在的作用机制.通过使用Morris水迷宫测试、Nissl染色、酶联免疫吸附试验等方法,本研究发现运动前菝葜皂苷元补充显著降低了高脂饮食诱导的大鼠逃避潜伏期,增加了穿越平台的次数,减轻了海马神经元损伤.此外,菝葜皂苷元补充也抑制了海马神经炎症,减少了 IL-1β、IL-6和TNF-α的水平.NF-κB的激活是高脂饮食导致的神经炎症的关键,而菝葜皂苷元能够降低NF-κB的磷酸化水平,从而抑制了炎症反应.此外,本研究还观察到菝葜皂苷元能够下调BACE1的表达,减少Aβ1-42的生成,为改善认知功能提供了分子基础.综上所述,本研究结果强调了运动前菝葜皂苷元在改善高脂饮食诱导认知障碍中的潜在应用和机制.
Abstract
This study aims to investigate the effects of A nemarrhena asphodeloides Bunge-derived Sarsasapogenin on cognitive function in high-fat diet-induced cognitive impairment rats and further explore its potential me-chanisms.Using methods including the Morris water maze test,Nissl staining,and enzyme-linked immunosorbent assay,our study found that pre-exercise supplementation of sarsasapogenin significantly reduced the escape latency and increased the number of platform crossings in high-fat diet-induced rats.This supplementation also alleviated hippocampal neuronal damage.Furthermore,sarsasapogenin supplementation inhibited hippocampal inflammation by reducing the levels of IL-1 β,IL-6,and TNF-α.The activation of NF-κB is a key factor in high-fat diet-induced neuroinflammation,and sarsasapogenin was found to decrease the phosphorylation of NF-κB,thereby suppressing the inflammatory response.Additionally,our study observed that sarsasapogenin downregulated the expression of B ACE 1,reducing the generation of Aβ 1-42,providing a molecular basis for the improvement of cognitive function.In summary,our study emphasizes the potential applications and mechanisms of pre-exercise sarsasapogenin sup-plementation in ameliorating high-fat diet-induced cognitive impairment.
关键词
知母(Anemarrhena/asphodeloides/Bunge)/菝葜皂苷元/高脂饮食/认知障碍Key words
Anemarrhena asphodeloides Bunge/Sarsasapogenin/High-fat diet/Cognitive impairment引用本文复制引用
出版年
2024
NETL
NSTL
维普
万方数据