Protection of Astragaloside Derivate on Oxidative Stress and Hypertrophy in Cardiomyocytes

Objective The astragaloside IV (ASI) has been proved to play an important role in protecting against cell death on cardiovascular diseases. This study aims to investigate the effect of the astragaloside derivate (ASId) on confronting oxidative stress and hypertrophy in myocardial cells. Methods Following exposure embryonic rat cardiac H9c2 cells to hydrogen peroxide (H2O2) and angiotensin II for developing oxidative stress and hypertrophy, ASId at final concentrations (0.1, 1, and 10 µmol/L) was added to study its role in protecting cardiomyocytes by biochemical detection and cell size measurement. In addition, the mitochondrial permeability transition pore (mPTP) opener atractyloside (20 µmol/L) and inhibitor cyclosporin A (CSA) (1 µmol/L) were employed to investigate the possible mechanisms for anti-oxidation. Results ASId at 1 and 10 μmol/L in cultures suppressed oxidative stress at different degrees, which induced the decrease in LDH activity and MDA content, and also the increase in SOD activity in comparable with the model group; The mPTP opener atractyloside and inhibitor CSA weakened and strengthened the role of ASId, respectively. ASId at 10 μmol/L inhibited cell hypertrophy, and the cell diameter, surface area, and protein content were all decreased in comparable of those cells in model group. Conclusion ASId is involved in the cytoprotective effects on oxidative stress through a pathway mediated by mPTP, and also has a protective effect against hypertrophy.