Cassia tora prevents Aβ1-42 aggregation, inhibits acetylcholinesterase activity and protects against Aβ1-42-induced cell death and oxidative stress in human neuroblastoma cells

Abstract

Background: Alzheimer's is a complex neurodegenerative disease and is characterized by extraneuronal accumulation of β-amyloid peptide. Because of its complex nature, multi-target directed ligands (MTDLs) are increasingly being considered as promising anti-Alzheimer therapeutic agents. This study is aimed at determining the effects of Cassia tora ethyl acetate fraction on several Alzheimer-associated deleterious events in test tubes as well as in human neuroblastoma SK-N-SH and SH-SY5Y cell lines.

Method: Ethyl acetate fraction of C. tora was purified by chromatography, characterized by ¹H and ¹³C NMR, and tested for its ability to prevent Aβ _1-42 aggregation by thioflavin-T fluorescence and transmission electron microscopy. We also analyzed the intracellular ROS level and cytotoxicity in SK-N-SH and SH-SY5Y cell lines.

Results: The extract inhibits the formation of Aβ _1-42 aggregation from monomers and oligomers, as also acetylcholinesterase activity, Aβ _1-42 -induced cell death, and Aβ _1-42 -dependent intracellular ROS production in both SK-N-SH and SH-SY5Y cells. In-depth chromatographic and spectroscopic analysis of the extract revealed that the active molecules are most likely triglycerides of oleic acid (C₁₈H₃₄O₂).

Conclusion: We demonstrate for the first time that Cassia tora fraction prevents Aβ _1-42 aggregation, inhibits acetylcholinesterase and alleviates Aβ _1-42 -induced oxidative stress in human neuroblastoma cells. We further suggest the possible use of triglycerides of oleic acid as efficient anti-Alzheimer agents.

Keywords: Acetycholinesterase; Alzheimer’s disease; Beta-amyloid; Cassia tora; Cell death; Oxidative stress.