Dexmedetomidine Relieves Myocardial Ischemia-Reperfusion Injury and Inhibits Apoptosis in Rats via the Janus Kinase 2/Signal Transducers and Activators of Transcription 3 Signaling Pathway

Abstract

To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. Rats were randomly assigned into sham, model, experimental and control groups. The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. Sham group only received threading without ligation. At 1 h before operation, 5.0 μg/kg dexmedetomidine and 5.0 μg/kg Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway agonist SC-39100 were intraperitoneally injected into experimental and control groups, respectively, while the same dose of normal saline was injected into sham and model groups. The left ventricular systolic pressure, left ventricular end-diastolic pressure, 1eft ventricular pressure rise (+dP/dtmax) and left ventricular pressure drop (-dP/dtmax) were measured using color Doppler ultrasonography. Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay was performed to detect cardiomyocyte apoptosis. The expression levels of phosphorylated Janus kinase 2 and phosphorylated signal transducers and activators of transcription 3 were determined using western blotting. Compared with sham group, model group had significantly decreased left ventricular systolic pressure, +dP/dtmax and -dP/dtmax and raised left ventricular end-diastolic pressure, cardiomyocyte apoptosis rate and phosphorylated Janus kinase 2 and phosphorylated signal transducers and activators of transcription 3 expressions (p<0.05). Experimental and control groups had significantly higher left ventricular systolic pressure, +dP/dtmax, -dP/dtmax and phosphorylated Janus kinase 2 and phosphorylated signal transducers and activators of transcription 3 expressions and lower left ventricular end-diastolic pressure and cardiomyocyte rate than those of model group (p<0.05). Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway.