Ligustrazine attenuates acute myocardium injury after thermal trauma

This study was designed to investigate the effects of ligustrazine on burn-induced myocardiac injury as well as TNF-α levels in severely burned rats. Sprague–Dawley rats were divided into four groups: (1) sham group, rats who underwent sham burn; (2) fluid-resuscitated sham group (FRsham), rats who underwent sham burn, and lactated Ringer's solution for resuscitation; (3) control group, rats given third-degree burns over 30% total body surface area (TBSA) and lactated Ringer's solution for resuscitation; (4) ligustrazine group, rats given burn and lactated Ringer's solution with ligustrazine inside for resuscitation. Myocardial injury was assessed at 6 h after burn by detecting serum levels of creatine kinase MB fraction (CK-MB) and lactate dehydrogenase (LDH), as well as water content, histological score, and ultrastructure change of cardiac tissue. In addition, myocardium ATP content was analyzed. Enzyme-linked immunosorbent assay (ELISA) was used to examine cardiac tumor necrosis factor-α (TNF-α) levels. The results showed that burn trauma resulted in the increasing serum LDH and CK-MB, elevated myocardial water content, aggravated myocardial histological and ultrastructural lesions, increased myocardium ATP, and serum TNF-α. Ligustrazine 10 mg/kg iv markedly inhibited increases in serum CK-MB and LDH, reduced myocardial water content from 76.91 ± 0.19% in control group to 75.40 ± 0.57%, significantly decreased the histologic scores of myocardium, and mollified the ultrastructural damage in cardiac myocytes. Ligustrazine significantly attenuated elevations in serum TNF-α level and myocardial ATP quantity. Therefore, our results demonstrate that ligustrazine exhibits significant protective effects on burn-induced myocardial injury via inhibiting the release of TNF-α and improving utilization of ATP.