Effect and mechanism of propofol on myocardial ischemia reperfusion injury in type 2 diabetic rats

• Model of myocardial ischemia and reperfusion injury in type 2 diabetic rats
• Propofol has a protective effect on diabetic rat hearts against I/R injury.
• Propofol attenuated endothelial cell dysfunction response to I/R.
• Propofol reduced apoptotic cell death following I/R in both normal and type 2 diabetic rats.

BackgroundPropofol has been reported to have an inhibitory effect on ischemia/reperfusion (I/R) injury in various experimental models by reducing oxidative stress, protecting mitochondrial function and suppressing apoptosis. The aim of this study was to investigate the effect and mechanism of propofol on myocardial I/R injury in type 2 diabetic rats.MethodsA total of 24 streptozotocin (STZ)-induced diabetic rats were randomly divided into three equal groups as follows: the DI group with myocardial I/R, which was induced by occluding the left anterior descending coronary artery for 30 min, followed by 2 h of reperfusion; the DP group, which underwent I/R and propofol infusion at 6 mg·kg− 1·h− 1; and the DC group, which underwent sham operations without tightening of the coronary sutures. As a control, 24 healthy, age-matched, male Wistar rats were randomly divided into three equal groups: the CI, CP and CC groups. The injured cardiac tissues were removed for microscopic examination after reperfusion. The serum concentrations of nitric oxide (NO) and endothelin (ET-1); the expression of Bax, Bcl-2 and Caspase-3 within the cardiac structures; and the number of apoptotic myocardial cells were measured.ResultsCompared with the baseline levels before ischemia, the serum concentration of ET-1 after 2 h of reperfusion was increased in the CI and DI groups, while the concentration of NO in these groups decreased after reperfusion. Compared with the I/R groups, propofol increased the content of NO and decreased the content of ET-1. Compared with the sham operation groups, I/R decreased the ratio of the anti-apoptotic protein Bcl-2 to the pro-apoptotic protein Bax, which resulted in an elevation of the index of apoptosis (AI). In contrast, compared with the I/R group, propofol increased the Bcl-2-to-Bax ratio and decreased the AI. I/R increased the expression of caspase-3 compared with the sham treatment groups, while treatment with propofol reduced caspase-3 expression relative to the I/R groups.ConclusionsThese data suggest that propofol can protect against myocardial ischemia–reperfusion injury in both normal and type 2 diabetic rats, possibly by attenuating endothelial cell injury and inhibiting the apoptosis of cardiomyocytes.