Melatonin relieves sepsis-induced myocardial injury via regulating JAK2/STAT3 signaling pathway.

Abstract

To study the effect of melatonin on myocardial injury of septic rats through regulating the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Healthy rats were selected as the samples and divided into blank group, sepsis group and sepsis + melatonin group. The difference in the myocardial tissue structure in the three groups of rats was observed via hematoxylin-eosin (HE) staining, and the messenger ribonucleic acid (mRNA) expression levels of JAK2 and STAT3 in myocardium were compared among groups through fluorescence quantitative polymerase chain reaction (qPCR). Western blotting was applied to detect the protein expressions of JAK2, phosphorylated (p)-JAK2, STAT3 and p-STAT3, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was utilized to determine the cell apoptosis in myocardial tissues. Moreover, the activity of superoxide dismutase (SOD) and content of malondialdehyde (MDA) in myocardial tissues as well as the activity of serum creatine kinase (CK) and lactate dehydrogenase (LDH) were measured and compared. There were inflammatory cells in the myocardium in sepsis group, and the pathological changes were milder in sepsis + melatonin group. The mRNA expressions of JAK2 and STAT3 and the protein expressions of JAK2, STAT3, p-JAK2 and p-STAT3 were raised remarkably in sepsis group compared with those in blank group and sepsis + melatonin group. The apoptosis rate in tissues was significantly different among the three groups, and it was the highest in sepsis group, followed by that in sepsis + melatonin group and blank group. There were significant differences in SOD activity and MDA content in myocardial tissues among the three groups, of which the SOD activity was the strongest in blank group, followed by that in sepsis + melatonin group and sepsis group, and the MDA content was the highest in sepsis group, followed by that in sepsis + melatonin group and blank group. Sepsis group had extremely notably increased activity of CK and LDH compared with blank group, while sepsis + melatonin group exhibited evidently decreased activity of CK and LDH in comparison with sepsis group. The JAK2/STAT3 signaling pathway is associated with sepsis-induced myocardial injury, and melatonin can relieve sepsis-induced myocardial injury by regulating the JAK2/STAT3 signaling pathway.