Abstract

To investigate the protective effect of melatonin (MLT) on myocardial injury in severely-burned rats and its mechanism. A total of 30 Sprague-Dawley (SD) rats were randomly assigned to three groups: sham group, burn group and MLT group, each n=10. The dorsal skin of animal was immersed into boiling water for 15 seconds to induce 30% total body surface area (TBSA) full-thickness burn, or immersed into 37 centigrade water for sham operation. Immediately after burn, the animals in burn group and MLT group were given intraperitoneally vehicle (1% alcohol in normal saline) or MLT (10 mg/kg) respectively. Six hours postburn, the blood from tail vessel was collected for serum preparation. After sacrificed, the myocardial tissues of rats were collected for the determination of malondialdehyde (MDA) and reduced glutathione (GSH) as well as glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) activities. Serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH) were also estimated. Compared with the sham control, burn injury increased MDA by 66.7% (1.55±0.17 nmol/mg vs. 0.93±0.05 nmol/mg) and decreased GSH by 27.8% (13.58±0.33 nmol/mg vs. 18.82±0.55 nmol/mg, both P<0.01) in myocardial tissues, GSH-Px activity was also slightly inhibited (74.04±3.42 nmol×min(-1)×mg(-1) vs. 93.79±3.76 nmol×min(-1)×mg(-1), P<0.05), but MPO level was found to increase to 2.8 folds (9.43±1.15 U/g vs. 3.41±0.27 U/g, P<0.01). These changes indicated the occurrence of oxidative stress in myocardial tissues after severe burn. MLT treatment relieved most of the abnormality with significant statistical significances (MDA: 0.89±0.08 nmol/mg vs. 1.55±0.17 nmol/mg, GSH: 17.23±0.54 nmol/mg vs. 13.58±0.33 nmol/mg, MPO: 6.91±0.51 U/g vs. 9.43±1.15 U/g, P<0.05 or P<0.01). In addition, the serum levels of CK and LDH in burn group increased to 37.8 folds and 7.4 folds respectively (both P<0.01). MLT treatment reduced CK by 32.9% and reduced LDH by 21.2% (P<0.05 and P<0.01). MLT treatment exerts the protective effect on myocardial injury in severely-burned rats, which is attributed predominantly to its inhibition on burn-induced oxidative stress injury.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call