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Neurodegenerative diseases, including Alzheimer’s disease, are prevalent in diabetic patients. DA-9801 is a standardized extract of Dioscorea japonica Thunb. and Dioscorea nipponica Makino, which has been shown to reduce blood glucose levels and exert protective effects against diabetic peripheral neuropathy. Here, we aimed to investigate whether DA-9801 could protect hyperglycemia-induced central neuropathy and to elucidate the underlying mechanisms. DA-9801 protected rat cortical primary neurons against hyperglycemia-induced neurotoxicity by lowering the levels of reactive oxygen species. In addition, we identified the genes whose expression in high glucose-treated primary neurons was significantly altered by DA-9801 treatment. Moreover, the major saponins of DA-9801, dioscin and protodioscin, protected neurons from hyperglycemia-induced toxicity, suggesting that these may be the most important active neuroprotective components of DA-9801. Our results showed that DA-9801 protects neurons derived from the central nervous system and that it may be useful to treat and delay the development of neurodegenerative diseases in diabetic patients.

Graphical abstract Highlights • DA-9801 protects rat primary cortical neurons from hyperglycemia-induced cytotoxicity. • DA-9801 reduces reactive oxidative species caused by high glucose treatment. • Microarray analysis reveals that DA-9801 regulates gene expression. • Dioscin and Protodioscin, the major saponins of DA9801, protect cortical neurons. Abstract Neurodegenerative diseases, including Alzheimer's disease, are prevalent in diabetic patients. DA-9801 is a standardized extract of Dioscorea japonica Thunb. and Dioscorea nipponica Makino, which has been shown to reduce blood glucose levels and exert protective effects against diabetic peripheral neuropathy. Here, we aimed to investigate whether DA-9801 could protect hyperglycemia-induced central neuropathy and to elucidate the underlying mechanisms. DA-9801 protected rat cortical primary neurons against hyperglycemia-induced neurotoxicity by lowering the levels of reactive oxygen species. In addition, we identified the genes whose expression in high glucose-treated primary neurons was significantly altered by DA-9801 treatment. Moreover, the major saponins of DA-9801, dioscin and protodioscin, protected neurons from hyperglycemia-induced toxicity, suggesting that these may be the most important active neuroprotective components of DA-9801. Our results showed that DA-9801 protects neurons derived from the central nervous system and that it may be useful to treat and delay the development of neurodegenerative diseases in diabetic patients. [ABSTRACT FROM AUTHOR]