Effects of endomorphin-1 postconditioning on myocardial ischemia/reperfusion injury and myocardial cell apoptosis in a rat model.

Endomorphins (EMs) have important roles in the body with regards to analgesia, feeding behavior, gastrointestinal movement and inflammatory reaction. Recent studies have reported that EMs may also participate in chronic hypoxia in the protection of rat myocardial ischemia/reperfusion; however, the mediator and underlying mechanisms remain to be elucidated. The aim of the present study was to investigate the effects of EM‑1 postconditioning on myocardial ischemia/reperfusion injury (MIRI) and myocardial cell apoptosis in a rat model, and to assess its likely mechanisms. A total of 48 male Sprague Dawley rats were randomly divided into four groups: Sham group, ischemia/reperfusion group (IR group), ischemic postconditioning group (IPO group) and EM‑1 postconditioning group (EM50 group). A MIRI model was established via occlusion of the left anterior descending branch of the coronary artery for 30 min, followed by reperfusion for 120 min in vivo. Hemodynamic indexes were recorded and analyzed. Following reperfusion, plasma lactate dehydrogenase (LDH), creatine kinase‑MB (CK‑MB), malondialdehyde (MDA), superoxide dismutase (SOD), interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) contents or activities were measured, infarct size was determined, and the expression levels of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) mRNA and cleaved caspase‑3 protein were assessed. In the IR group, mean arterial pressure (MAP) and heart rate (HR) were decreased compared with in the sham group. In addition, LDH and CK‑MB levels were increased; IL‑6, TNF‑α and MDA content was increased; SOD activity was decreased; the Bcl‑2/Bax ratio was decreased; and cleaved caspase‑3 protein expression levels were increased in the IR group. Compared with in the IR group, in the IPO and EM50 groups, MAP and heart rate (HR) were recovered to various extents post‑reperfusion; LDH and CK‑MB levels were decreased; IL‑6, TNF‑α and MDA content was decreased; SOD activity was increased; infarct size was reduced; the Bcl‑2/Bax ratio was increased; and cleaved caspase‑3 protein expression levels were decreased. In conclusion, EM‑1 postconditioning was revealed to reduce I/R injury and inhibit myocardial cell apoptosis, which may be associated with reductions in oxidative stress and inflammatory reactions.