Moscatilin can protect rat pheochromocytoma cells against methylglyoxal-induced damage.\nElimination of the effect of advanced glycation end-products (AGEs) but activation of AMP-activated\nprotein kinase (AMPK) are the potential therapeutic targets for the neurodegenerative diseases.\nOur study aimed to clarify AMPK signalingâ??s role in the beneficial effects of moscatilin on the\ndiabetic/hyperglycemia-associated neurodegenerative disorders. AGEs-induced injury in SH-SY5Y\ncells was used as an in vitro neurodegenerative model. AGEs stimulation resulted in cellular\nviability loss and reactive oxygen species production, and mitochondrial membrane potential collapse.\nIt was observed that the cleaved forms of caspase-9, caspase-3, and poly (ADP-ribose) polymerase\nincreased in SH-SY5Y cells following AGEs exposure. AGEs decreased Bcl-2 but increased Bax\nand p53 expression and nuclear factor kappa-B activation in SH-SY5Y cells. AGEs also attenuated\nthe phosphorylation level of AMPK. These AGEs-induced detrimental effects were ameliorated by\nmoscatilin, which was similar to the actions of metformin. Compound C, an inhibitor of AMPK,\nabolished the beneficial effects of moscatilin on the regulation of SH-SY5Y cellsâ?? function, indicating\nthe involvement of AMPK. In conclusion, moscatilin offers a promising therapeutic strategy to\nreduce the neurotoxicity or AMPK dysfunction of AGEs. It provides a potential beneficial effect with\nAGEs-related neurodegenerative diseases.
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