and its compounds suppress hydrogen peroxide-induced oxidative stress in HT22 cells.

UNLABELLED

This study aimed to explore the protective effects of (EA) leaves and its compounds on hydrogen peroxide (HO)-induced neuronal cell death. EA effectively reversed the HO-induced decrease in HT22 cell viability. Anti-apoptotic marker poly(ADP-ribose) polymerase significantly increased with EA treatment, whereas BAX/BCL2 and cleaved caspase-3/procaspase-3 ratios, which represent apoptotic markers, were dose-dependently decreased by EA treatment. Additionally, EA effectively decreased β-secretase production, acetylcholine esterase activity, and Tau phosphorylation, pathological features observed in Alzheimer's disease. Furthermore, EA significantly increased the protein levels of NRF2 and HO-1, as well as the gene expression of antioxidant enzymes, including catalase, superoxide dismutase 1, and glutathione peroxidase. LC-MS/MS and HPLC analyses revealed the presence of chlorogenic acid and leucosides in EA. Both chlorogenic acid and leucosides showed protective effects against HO-induced neuronal cell death. This study highlights the potential of EA and its compounds as functional edible agents for neuroprotection against oxidative stress.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s10068-024-01601-4.