title: Ligustrazine attenuates acute myocardium injury after thermal trauma.
abstract: This study was designed to investigate the effects of ligustrazine on burn-induced myocardiac injury as well as TNF-alpha 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 6h 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-alpha (TNF-alpha) 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-alpha. Ligustrazine 10mg/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-alpha 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-alpha and improving utilization of ATP.
authors.affiliation: Department of Pharmacology, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, PR China.
authors.forename: Shan
authors.initials: S
authors.lastname: Gao
authors.forename: Zhi-Wu
authors.initials: ZW
authors.lastname: Chen
authors.forename: Hong
authors.initials: H
authors.lastname: Zheng
authors.forename: Xu-Lin
authors.initials: XL
authors.lastname: Chen
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002056:Burns; D006335:Heart Injuries / Q000188:drug therapy* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000648:ultrastructure; D011719:Pyrazines / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014665:Vasodilator Agents / Q000627:therapeutic use*; D014867:Water / Q000378:metabolism
chemical_list: D011719:Pyrazines; D014409:Tumor Necrosis Factor-alpha; D014665:Vasodilator Agents; D014867:Water; D000255:Adenosine Triphosphate; C017953:tetramethylpyrazine