Protective effect of astragaloside IV on adriamycin-induced HL-1 cell injury and its mechanism

AIM To investigate the protective effect of astragaloside IV (ASIV) on doxorubicin-induced HL-1 cell injury and its related mechanism, and to provide cardiac therapy for doxorubicin-induced myocardial injury.

METHODS HL-1 cardiomyocytes were divided into normal control group, model group, 1 μmol/L ASIV group, 2 μmol/L ASIV group and 4 μmol/L ASIV group. The myocardial cell injury model was made with DOX solution of 5.2 μmol/L and cultured in a cell incubator for 12h. ASIV solutions of 1 μmol/L, 2 μmol/L and 4 μmol/L were added into the culture bottles of the corresponding groups and then they were placed into the cell culture box for culture. After 12 hours, the ASIV solutions were removed to detect the relevant indexes. CCK8 method was used to determine the concentration of adriamycin modeling drug, flow cytometry was used to observe the concentration of adriamycin modeling time, and fluorescence staining was used to detect the level of apoptosis, mitochondrial membrane potential and ROS of adriamycin induced HL-1 cardiomyocytes by ASIV. The content of NO in the supernatant of adriamycin induced HL-1 cardiomyocytes was detected by spectrophotometry.

RESULTS The model concentration of adriamycin was 5.2 μmol/L. The apoptosis time of HL-1 myocardial cells induced by adriamycin was 12h. After adriamycin administration, apoptosis was significantly increased in model group (P<0.01) and it significantly decreased in 2 μmol/L and 4 μmol/L ASIV groups (P<0.01). Compared with those in model group, ROS expression was decreased and NO concentration and mitochondrial intima potential were increased in ASIV treatment groups. In 4 μmol/L ASIV group, ROS concentration was significantly decreased, while NO concentration and mitochondrial intima potential were significantly increased (P<0.05).

CONCLUSION ASIV may inhibit adriamycin induced cardiomyocyte apoptosis in a dose-dependent manner by reducing the decline of membrane potential of cardiomyocytes, reducing ROS expression, increasing NO content, and alleviating oxidative stress injury.