The Effect and Mechanism of Hyperoside on High Glucose-induced Oxidative Stress Injury of Myocardial Cells

OBJECTIVE:To explore the effect and mechanism of hyperoside on high glucose-induced oxidative stress injury of myocardial cells.METHODS:Oxidative stress injury of myocardial cells was simulated by treating with high glucose. Cells were divided into five groups: control group (5.5 mmol/L glucose); high glucose model group (35 mmol/L glucose); hyperoside protection groups (35 mmol/L glucose +4, 8, 20 nmol/L hyperoside). Cells were incubated for 48 h. The cell viability was detected by CCK-8. Apoptosis was measured through flow cytometry. The level of ROS was tested by Reactive Oxygen Species Assay Kit DCFH-DA with flow cytometer. The level of SOD and MDA was detected by SOD Assay Kit and MDA Assay Kit respectively. The protein levels of phosphatidylinositide 3-kinases (PI3K), protein kinase B (AKT), p-AKT, nuclear factor erythroid 2-related factor 2 (Nrf2) and p-Nrf2 were detected by Western blot. The activation of AKT was analyzed by immunofluorescence staining.RESULTS:Compared with control group, the cell viability, the levels of SOD, the expression of PI3K, the ratio of p-AKT/AKT and p-Nrf2/Nrf2 and the percentage of AKT positive cells in high glucose group were decreased with enhancive apoptosis and levels of ROS and MDA (P<0.05). Compared with high glucose group, the cell viability, the levels of SOD, the expression of PI3K, the ratio of p-AKT/AKT and p-Nrf2/Nrf2 and the percentage of AKT positive cells in hyperoside group (4, 8, 20 nmol/L) were increased with reduced apoptosis and levels of ROS and MDA (P<0.05).CONCLUSION:Hyperoside protects myocardial cells against oxidative stress injury via activation of PI3K/AKT/Nrf2 signal pathway.