Gastrodin protects myocardial cells against hypoxia/reoxygenation injury in neonatal rats by inhibiting cell autophagy through the activation of mTOR signals in PI3K-Akt pathway.

Abstract

This study aimed to investigate the protective effect of gastrodin (GAS) on myocardial cells with hypoxia/reoxygenation (H/R) injury in neonatal rats and explore the underlying mechanism. Myocardial cells were extracted from neonatal rats and divided into six groups: control, H/R, H/R + Low-Concentration GAS, H/R + Middle-Concentration GAS, H/R + High-Concentration GAS and H/R + High-Concentration GAS + AKT Inhibitor groups. After 48-h treatment, cell viability, autophagosome quantity and the expression levels of LC3-II, p62, Akt, pAkt, mammalian target of rapamycin (mTOR) and uncoordinated 51-like kinase 1 (ULK1) in myocardial cells were made comparisons among each group. Gastrodin improved the proliferation activity of myocardial cells under H/R injury in a dose-dependent manner and inhibited the level of cell autophagy. However, when AKT inhibitor was added, the effect of GAS was partly inhibited (P < 0.05). Gene and protein expressions showed that GAS made no significant effect on the expression quantity of Akt and mTOR genes (P > 0.05) but could significantly promote the phosphorylation of Akt and mTOR (P < 0.05). GAS had significant inhibiting effect on the expression of ULK1 (P < 0.05). Gastrodin could protect against H/R injury of myocardial cells in neonatal rats by reducing the level of autophagy through the activation of mTOR signals in PI3K-Akt pathway.