title: Ethyl pyruvate protects against sepsis by regulating energy metabolism.
abstract: BACKGROUND
  Ethyl pyruvate (EP) is a derivative of pyruvic acid that has been demonstrated to be a potential scavenger of reactive oxygen species as well as an anti-inflammatory agent. In this study, we investigated the protective effects of EP and its role in regulating the energy metabolism in the livers of cecal-ligation-and-puncture-induced septic mice.
  
  
  METHODS
  The animals were treated intraperitoneally with 0.2 mL of Ringer's lactate solution or an equivalent volume of Ringer's lactate solution containing EP immediately after cecal ligation and puncture. Each mouse in the Sham group was only subjected to a laparotomy. At 30-, 60-, 180-, and 360-minute time points, we measured the histopathological alterations of the intestines, and the plasma levels of interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor-α, and the total antioxidative capacity, malondialdehyde content, and lactate and lactate/pyruvate levels in livers. Furthermore, we detected the levels of adenosine triphosphate, total adenylate, and energy charge in the livers.
  
  
  RESULTS
  Our results demonstrated that the administration of EP significantly improved the survival rate and reduced intestinal histological alterations. EP inhibited the plasma levels of IL-1β, IL-6, and tumor necrosis factor-α and increased the IL-10 level. EP significantly inhibited the elevation of the malondialdehyde, lactate, and lactate/pyruvate levels and enhanced the total antioxidative capacity levels in the liver tissues. The downregulation of the adenosine triphosphate, total adenylate, and energy charge levels in the liver tissues was reversed in the septic mice treated with EP.
  
  
  CONCLUSIONS
  The results suggest that EP administration effectively modulates the energy metabolism, which may be an important component in treatment of sepsis.
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Hongjun
authors.initials: H
authors.lastname: Kang
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Mao
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Critical Care Medicine, The Centre Hospital of BaoTou, BaoTou, People's Republic of China.
authors.forename: Ting
authors.initials: T
authors.lastname: Yin
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Song
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Liang
authors.initials: L
authors.lastname: Pan
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Xin
authors.initials: X
authors.lastname: Hu
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Jie
authors.initials: J
authors.lastname: Hu
authors.affiliation: Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Feihu
authors.initials: F
authors.lastname: Zhou
keywords: energy metabolism; ethyl pyruvate; inflammation; reactive oxygen species; sepsis