Abstract: Objective    To explore the mechanism of dexmedetomidine reducing myocardial ischemia-reperfusion injury and inhibiting apoptosis and its regulation signaling of janus kinase 2/signaltransducer and activator of transcription 3 (JAK2/STAT3) signaling pathway.   Methods    Rat were randomly divided into the following 4 groups: a sham operation group, a model group, an experimental group, and a control group. The anterior descending branch of the left tubular artery was ligated to construct an ischemia-reperfusion rat model. The sham operation group only threaded without ligation. The rats in the experimental group and in the control group were intraperitoneally injected with 5.0 μg/kg dexmedetomidine and JAK2/STAT3 signaling pathway agonist SC-39100 1 h before surgery, and the rats in the sham group and model group were injected with equal doses of normal saline. Cardiac ultrasonography was used to examine the left ventricular systohc pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and left ventricular pressure rise rate (1eft ventricular pressure rise, +dp/dtmax) and the maximum rate of left ventricular pressure drop (1eft ventricular pressure drop, -dp/dtmax). TUNEL staining was used to detect the apoptosis of myocardial cells. DCFH-DA staining was used to detect the level of ROS in the myocardium. Western blot was used to detect the expression levels of p-JAK2 and p-STAT3 in rat myocardium. Results   Compared with the sham group, the LVSP, +dp/dtmax, -dp/dtmax of the model group significantly reduced, and the LVEDP, the myocardial apoptosis rate, the fluorescence intensity of ROS, the expression of p-JAK2, and p-STAT3 significantly increased, with statistical differences  (P<0.05). Compared with the model group, the LVSP, +dp/dtmax, -dp/dtmax, the expression of p-JAK2, p-STAT3 in the experimental group and the control group obvious increased, the LVEDP, the myocardial apoptosis rate, the fluorescence intensity of ROS significantly decreased, with statistical differences (P<0.05).    Conclusions   Pretreatment with dexmedetomidine can significantly reduce myocardial ischemia-reperfusion injury and reduce cardiomyocyte apoptosis, which may be related to the activation of JAK2 / STAT3 signal and inhibition of oxidative stress.

Key words: Dexmedetomidine; ,  , Myocardial ischemia-reperfusion injury; ,  , Cell apoptosis, Janus kinase 2/signaltransducer and activator of transcription 3 signaling pathway