Ginger leaf polyphenols mitigate β-amyloid toxicity via JNK/FOXO pathway activation in Caenorhabditis elegans.

Abstract

β-Amyloid (Aβ) aggregation is the major pathological feature of Alzheimer's disease (AD), resulting in oxidative stress and further exacerbating Aβ aggregation. Ginger leaf polyphenols (GLP) have been found to possess antioxidant activity, evidencing their potential in addressing AD. GLP is mainly composed of 12 polyphenols, 8 organic acids, and 6 glycosides, of which polyphenols are predominantly composed of apigenin, kaempferol, and quercetin derivatives. Moreover, GLP alleviates reproductive toxicity, longevity toxicity, and neurotoxicity induced by Aβ via regulating the antioxidase system in Caenorhabditis elegans. As shown by the network pharmacology results, GLP might activate the JNK/Foxo signaling pathway to regulate the antioxidase system, which was evidenced by the up-regulation of gene expression levels of jnk-1, daf-16, sod-3, and hsp-16.2. Overall, GLP might be a potential antioxidant for combating AD.