Hydromorphone Alleviates Myocardial Ischemia-reperfusion Injury in Rats via Regulating TLR-4/NF-κB Pathway and Apoptosis-related Protein Expressions

The purpose of this work was to investigate the effect of hydromorphone preconditioning on inflammatory response, oxidative stress, Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-kappa B) pathway, and apoptosis-related protein expression in rats with myocardial ischemia-reperfusion injury (MIRI). Fifty-four healthy rats were divided into sham-operated, model and treated groups. The MIRI model was established in model and treated groups. At 10 min before the molding, the treated group was injected with 0.2 mg/kg hydromorphone hydrochloride. At the end of reperfusion, compared with model group, in treated group the left ventricular systolic pressure, maximum rate of left ventricular pressure rise and fall were increased, the left ventricular end-diastolic pressure was decreased, the serum creatine kinase isoenzyme, lactate dehydrogenase and troponin T levels and myocardial infarction rate were decreased, the serum interleukin 6 and malondialdehyde levels were decreased, the serum interleukin 10 and superoxide dismutase levels were increased, the myocardial TLR-4, NF-kappa B p65, B-cell lymphoma-2 associated X (Bax) and cysteinyl aspartate specific proteinase-3 (Caspase-3) protein expression levels were decreased, and the myocardial B-cell lymphoma-2 (Bcl-2) protein expression level was increased. In conclusion, hydromorphone can alleviate the MIRI in rats via reducing inflammatory response and oxidative stress and down-regulating TLR-4/NF-kappa B pathway and Bcl-2, Bax and Caspase-3 expressions.