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<p>Chicoric acid (CA) is a type of hydroxycinnamic acid that has been regarded as a functional ingredient given its health benefits for the treatment of Alzheimer’s disease (AD). In this study, free radical-scavenging capacities of CA were enhanced in a dose-dependent manner, after which the protective effects of CA against amyloid-beta (Aβ)-induced neurotoxicity in SH-SY5Y cells was investigated. CA suppressed Aβ<sub>25–35</sub>-induced increase in the production of reactive oxygen species. Stimulation with Aβ<sub>25–35</sub> enhanced the protein expression of β-secretase and presenilin proteins, which were subsequently inhibited by CA. CA also affected the levels of low-density lipoprotein receptor-related protein-1 and receptor for advanced glycation endproducts, both of which are related to blood–brain barrier function. Furthermore, Aβ exposition downregulated insulin-degrading enzyme and neprilysin protein expressions, which were reversed by CA. Overall, the results suggest that CA may protect against Aβ-induced neurotoxicity via modulating Aβ generation and transportation.</p>

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Free radical-scavenging and anti-amyloidogenic properties of chicoric acid

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月11日

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  • Mei Tong He,
  • Eun Ju Cho,
  • Ji-Hyun Kim,
  • Hyun Young Kim

摘要

Chicoric acid (CA) is a type of hydroxycinnamic acid that has been regarded as a functional ingredient given its health benefits for the treatment of Alzheimer’s disease (AD). In this study, free radical-scavenging capacities of CA were enhanced in a dose-dependent manner, after which the protective effects of CA against amyloid-beta (Aβ)-induced neurotoxicity in SH-SY5Y cells was investigated. CA suppressed Aβ25–35-induced increase in the production of reactive oxygen species. Stimulation with Aβ25–35 enhanced the protein expression of β-secretase and presenilin proteins, which were subsequently inhibited by CA. CA also affected the levels of low-density lipoprotein receptor-related protein-1 and receptor for advanced glycation endproducts, both of which are related to blood–brain barrier function. Furthermore, Aβ exposition downregulated insulin-degrading enzyme and neprilysin protein expressions, which were reversed by CA. Overall, the results suggest that CA may protect against Aβ-induced neurotoxicity via modulating Aβ generation and transportation.