Spiraeoside protects human cardiomyocytes against high glucose‐induced injury, oxidative stress, and apoptosis by activation of PI3K/Akt/Nrf2 pathway
Hongyang Liu, Zhiyong Zhang, Lei Zhang, Xinliang Yao, Xiaoming Zhong, Guanchang Cheng, Lefeng Wang, Qilin Wan
Abstract
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.