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

The aggregation of beta-amyloid (A beta) has the neurotoxicity, which is thought to play critical role in the pathogenesis of Alzheimer's disease (AD). Inhibiting A beta 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 A beta(1-42) transgenic Caenorhabditis elegans (C. elegans). The results showed that DISS (5 and 50 mu M) treatment significantly prolonged the life span, increased the number of egg-laying, reduced paralysis rate, decreased the levels of lipofuscin and ROS and attenuated A beta deposition in A beta(1-42) 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 A beta(1-42) transgenic C. elegans. These results suggested that DISS has the protective effect against A beta(1-42)-induced pathological damages and prolongs the life span of C. elegans, which may be related to the reduction of A beta deposition and neurotoxicity by regulating expression of genes related to antioxidation and autophagy.