Abstract

To investigate the expression of autophagy markers of brain cells and the effect of propofol on autophagy during myocardial ischemia-reperfusion in type 2 diabetic rats. 36 healthy male Sprague Dawley rats were randomly divided into 6 groups, 6 in each group, fed with high-sugar and high-fat diet for 8 w and intraperitoneal injection of streptozotocin to prepare the rat model of type 2 diabetes. The 6 groups are: diabetic rat with sham operation group, diabetic rat with myocardial ischemia reperfusion group, diabetic rat with myocardial ischemia reperfusion+propofol group, normal rat with sham operation, normal rat with myocardial ischemia reperfusion group, normal rat with myocardial ischemia reperfusion+propofol group[1]. In the normal rat with myocardial ischemia reperfusion+propofol group and diabetic rat with myocardial ischemia reperfusion+ propofol group, the left anterior descending coronary artery was ligated for 30 min and reperfused for 2 h after the propofol was injected with 6 mg•kg-1•h-1 for 10 min. Normal rat with myocardial ischemia reperfusion group and diabetic rat with myocardial ischemia reperfusion groups were pumped with 3 ml•kg-1•h-1 normal saline for 10 min, followed by ligation of the left anterior descending coronary artery for 30 min and reperfusion for 2 h. Arterial ligation was not performed in the normal rat with sham operation group and diabetic rat with sham operation groups. Brain tissue was taken to detect its levels of mechanistic target of rapamycin, phosphorylated mammalian target of rapamycin and Beclin-1 by Western blot. Compared with normal rat with sham operation group, phosphorylated mammalian target of rapamycin level was significantly decreased, and mechanistic target of rapamycin beclin-1 expression level was significantly increased in the other 5 groups (p<0.05). Compared with diabetic rat with myocardial ischemia reperfusion group, the expression level of phosphorylated mammalian target of rapamycin in diabetic rat with myocardial ischemia reperfusion+propofol group was increased, while beclin-1 and mechanistic target of rapamycin expression levels were significantly decreased (p<0.05). Compared with normal rat with myocardial ischemia reperfusion group, the level of mechanistic target of rapamycin in normal rat with myocardial ischemia reperfusion+propofol group was significantly increased, while the beclin-1 and mechanistic target of rapamycin expression levels were significantly decreased (p<0.05). Diabetes can promote the autophagy of brain cells during myocardial ischemia-reperfusion and aggravate the brain injury. Propofol can up-regulate the level of Phosphorylated mammalian target of rapamycin and down-regulate the expression of mechanistic target of rapamycin to alleviate the damage of brain cells after myocardial ischemia and reperfusion in normal rats and type 2 diabetic rats.