Peptides from sesame cake reduce oxidative stress and amyloid-β-induced toxicity by upregulation of SKN-1 in a transgenic Caenorhabditis elegans model of Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is a serious worldwide public health problem. Its pathogenesis is believed to be driven by amyloid-β (Aβ)-induced oxidative stress and toxicity. We investigated the effects of peptides from sesame cake (PSC), a novel bioactive by-product of sesame processing, on Aβ-induced toxicity and oxidative stress, in a transgenic AD Caenorhabditis elegans model. Dietary supplementation with PSC prolonged the lifespan, increased locomotion, and delayed paralysis compared with a control group. PSC also enhanced oxidative stress resistance, reduced ROS levels and Aβ deposition, and upregulated mRNA expression levels of key antioxidant enzyme genes. The downregulation of skn-1 blocked the PSC-mediated protective effect in AD nematodes. Taken together, these data indicate that treatment with PSC reduced oxidative stress, thereby reducing Aβ-induced toxicity in transgenic C. elegans, and these effects were mediated via skn-1, implying that PSC may have potential as a nutraceutical in the prevention of AD-related oxidative stress complications.

Keywords

• Peptides from sesame cake
• Caenorhabditis elegans
• Alzheimer’s disease
• Amyloid-β
• Oxidative stress
• SKN-1