Background & objectives: Amyloid β-peptide (Aβ) has been shown to be responsible for senile plaque formation and cell damage in Alzheimer's disease (AD). This study was aimed to explore the role of natural compound icariin on the aggregation and the cytotoxicity of Aβ in vitro.
Methods: Thioflavin T (ThT) fluorescence assay and transmission electron microscopy (TEM) imaging were done to determine the influence of icariin on the aggregation of Aβ1-42 peptide. MTT assay was used to evaluate the protective effect of icariin on Aβ1-42 induced cytotoxicity in neuroblastoma SH-SY5Y cells.
Results: Icariin inhibited Aβ1-42 aggregation in a dose-dependent manner. Additionally, icariin also prevented the cytotoxicity of Aβ1-42 in SH-SY5Y cells by decreasing the production of peroxide hydrogen during the aggregation of this peptide.
Interpretation & conclusions: The results indicated a novel antagonistic role of icariin in the neurotoxicity of Aβ1-42 via inhibiting its aggregation, suggesting that icariin might have potential therapeutic benefits to delay or modify the progression of AD.