[Astragaloside â
£'s Therapeutic Effect on Myocardial Infarction via Affecting Autophagy and the Mechanism Study].
Sichuan Da Xue Xue Bao Yi Xue Ban
; 52(2): 222-228, 2021 Mar.
Article
em Zh
| MEDLINE
| ID: mdl-33829695
ABSTRACT
OBJECTIVE:
The purpose of this study was to investigate the protective effect of astragaloside â £ (AS-â £) 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-â £ (0.1 µmol/L AS-â £), H/R-medium AS-â £ (1 µmol/L AS-â £), H/R-high AS-â £ (10 µmol/L AS-â £) and H/R-high AS-â £-AKT (10 µmol/L AS-â £+5 µmol/L AKT) groups. After 48 h of treatment, the contents of LC3-â ¡, 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-â £ improved the proliferative activity of cardio AS-â £ 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-â £ was partially inhibited ( P<0.05). Gene and protein expression showed that AS-â £ 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 - â £ can reverse H/R injury induced the expression of autophagy body P62.CONCLUSION:
AS-â £ 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.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fosfatidilinositol 3-Quinases
/
Infarto do Miocárdio
Limite:
Animals
Idioma:
Zh
Ano de publicação:
2021
Tipo de documento:
Article