AIM To investigate the molecular pharmacological mechanism of Salidroside in protecting rat heart injury induced by high altitude hypoxia.
METHODS Wistar rats were randomly divided into 5 groups: blank control group (1 500 m), hypoxic saline group (6 500 m+NS), hypoxia compound C group (6 500 m+comC), hypoxia salidroside group(6 500 m+Sal), hypoxia salidroside+ compound C group (6 500 m+comC+Sal).
RESULTS After exposure to hypoxic environment, myocardial structure was changed and myocardial apoptosis was aggravated(P<0.05). Salidroside treatment could improve the pathological damage of myocardial cells and reduce the degree of myocardial apoptosis(P<0.05); At the same time, the level of phosphorylated AMPK increased and the level of phosphorylated mTOR decreased(P<0.05). The expression levels of AMPK and mTOR were between compound C group and salidroside group, but the expression of autophagy protein Beclin-1 was higher than that of compound C group(P<0.05).
CONCLUSION salidroside can positively regulate AMPK signaling pathway, activate autophagy and protect myocardium from hypoxia injury.