[Astragaloside â £'s Therapeutic Effect on Myocardial Infarction via Affecting Autophagy and the Mechanism Study].

OBJECTIVE: The purpose of this study was to investigate the protective effect of astragaloside ⠣ (AS-⠣) on neonatal rats' hypoxic/reoxygenated (H/R) injured myocardial cells and to explore its underlying mechanism. METHODS: Cardiac cells were extracted from newborn rats and divided into control, H/R, H/R-low AS-⠣ (0.1 μmol/L AS-⠣), H/R-medium AS-⠣ (1 μmol/L AS-⠣), H/R-high AS-⠣ (10 μmol/L AS-⠣) and H/R-high AS-⠣-AKT (10 μmol/L AS-⠣+5 μmol/L AKT) groups. After 48 h of treatment, the contents of LC3-⠡, p62, AKT, pAKT, rapamycin (mTOR) mammalian targets and uncoordinated 51-like kinase 1 (ULK1) in cardiac myocytes were compared. Immunofluorescence staining was used to detect the expression of P62 in myocardium autophagosome. RESTULTS: AS-⠣ improved the proliferative activity of cardio AS-⠣ improved the proliferative activity of cardiomyocytes in H/R injury in a dose-dependent manner and inhibited the level of cell autophagy. However, when AKT inhibitors were added, the effect of AS-⠣ was partially inhibited ( P<0.05). Gene and protein expression showed that AS-⠣ had no significant effect on the expression of AKT and mTOR genes ( P>0.05), but could significantly promote the phosphorylation of AKT and mTOR ( P<0.05). Immunofluorescence staining results showed that high concentrations of the AS - ⠣ can reverse H/R injury induced the expression of autophagy body P62. CONCLUSION: AS-⠣ showed protection effect on H/R injured myocardial cells. The possible mechanism is by reducing the autophagy level via activating the mTOR signal in the PI3K/AKT pathway, thereby preventing H/R damage in neonatal rat cardiomyocytes.