Objective: The aim of this study was to investigate the role of dexmedetomidine (Dex) in lactate signaling cascade and myocardial ischemia/reperfusion (I/R) injury in mice.
Materials and methods: The left anterior descending of the coronary artery was ligatured for 30 min and then reperfused for 6 h to induce myocardial I/R injury in mice. Heart samples were collected and the levels of lactate, SOD and MDA were measured. Infarct size and myocardium were stained with triphenyltetrazolium chloride and TUNEL, respectively. In addition, the expression levels of MCT1, cytochrome c, cleaved caspase-9 and -3 were detected by Western blot.
Results: The myocardial infarct size, lactate and MDA levels of the I/R group were significantly increased, whereas the SOD activity was decreased. However, Dex significantly reduced the myocardial infarct size, as well as lactate and MDA levels in contrast to the I/R group. Meanwhile, the SOD activity was remarkably increased. The expression levels of MCT1, cytochrome c, cleaved caspase-9 and -3 were significantly increased in the I/R group. In addition, Dex administration further increased the expression of MCT1, whereas decreased the expressions of cytochrome c, cleaved caspase-9 and -3 in contrast to the I/R group.
Conclusions: Dex elevated the expression of mitochondrial MCT1 and inhibited oxidative stress and the activation of mitochondria-dependent apoptosis in mice. This indicated that Dex attenuated myocardial I/R injury by regulating lactate signaling cascade.