The present study aimed to explore the effect of spiraeoside, an active quercetin glucoside, on diabetic cardiomyopathy in vitro. Our results showed that spiraeoside attenuated high glucose (HG)-induced reduction of cell viability and increased myocardial enzymes lactate dehydrogenase and aspartate aminotransferase in AC16 cells. Spiraeoside exerted antioxidant activity in HG-induced AC16 cells as spiraeoside inhibited reactive oxygen species and malondialdehyde production and increased activities of superoxide dismutase, glutathione peroxidase, and catalase. Spiraeoside prevented HG-induced apoptosis of AC16 cells. HG stimulation-caused the decrease in the expression levels of p-Akt, nuclear Nrf2, and HO-1 was elevated after spiraeoside treatment in AC16 cells. However, the effects of spiraeoside were reversed by LY294002. In conclusion, spiraeoside protected AC16 cells against HG-induced oxidative stress, cell injury, and apoptosis. The protective effect of spiraeoside was regulated by the PI3K/Akt/Nrf2 signaling pathway.
Keywords: PI3K/Akt/Nrf2; diabetic cardiomyopathy; high glucose; oxidative stress; spiraeoside.
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