3,6'-disinapoyl sucrose attenuates Aβ1-42 - induced neurotoxicity in Caenorhabditis elegans by enhancing antioxidation and regulating autophagy.

Abstract

The aggregation of β-amyloid (Aβ) has the neurotoxicity, which is thought to play critical role in the pathogenesis of Alzheimer's disease (AD). Inhibiting Aβ deposition and neurotoxicity has been considered as an important strategy for AD treatment. 3,6'-Disinapoyl sucrose (DISS), one of the oligosaccharide esters derived from traditional Chinese medicine Polygalae Radix, possesses antioxidative activity, neuroprotective effect and anti-depressive activity. This study was to explore whether DISS could attenuate the pathological changes of Aβ1-42 transgenic Caenorhabditis elegans (C. elegans). The results showed that DISS (5 and 50 μM) treatment significantly prolonged the life span, increased the number of egg-laying, reduced paralysis rate, decreased the levels of lipofuscin and ROS and attenuated Aβ deposition in Aβ1-42 transgenic C. elegans. Gene analysis showed that DISS could up-regulate the mRNA expression of sod-3, gst-4, daf-16, bec-1 and lgg-1, while down-regulate the mRNA expression of daf-2 and daf-15 in Aβ1-42 transgenic C. elegans. These results suggested that DISS has the protective effect against Aβ1-42 -induced pathological damages and prolongs the life span of C. elegans, which may be related to the reduction of Aβ deposition and neurotoxicity by regulating expression of genes related to antioxidation and autophagy.

• Authors: Xiaoli Tang, Yuming Zhao, Yanan Liu, Yang Liu, Yue Liu, Fenxi Niu, Fang Fang
• Journal: Journal of cellular and molecular medicine (J Cell Mol Med) Vol. 26 Issue 4 Pg. 1024-1033 (02 2022) ISSN: 1582-4934 [Electronic] England
• PMID: 35044105 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

Chemical References

• Amyloid beta-Peptides
• Antioxidants
• Peptide Fragments
• amyloid beta-protein (1-42)
• Sucrose

Topics

• Alzheimer Disease (drug therapy, genetics, metabolism)
• Amyloid beta-Peptides (genetics, toxicity)
• Animals
• Antioxidants (metabolism, pharmacology)
• Autophagy
• Caenorhabditis elegans (genetics, metabolism)
• Disease Models, Animal
• Peptide Fragments
• Sucrose (metabolism)