Ethyl Pyruvate Has Anti-Inflammatory and Delayed Myocardial Protective Effects after Regional Ischemia/Reperfusion Injury.
10.3349/ymj.2010.51.6.838
- Author:
In Seok JANG
1
;
Mi Young PARK
;
Il Woo SHIN
;
Ju Tae SOHN
;
Heon Keun LEE
;
Young Kyun CHUNG
Author Information
1. Department of Cardiothoracic and Vascular Surgery, Institute of Health Sciences, Gyeongsang National University, Jinju, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Ethyl pyruvate;
myocardium;
reperfusion injury;
inflammation
- MeSH:
Animals;
Anti-Inflammatory Agents/*pharmacology;
Cell Nucleus/metabolism;
Cytoplasm/metabolism;
Heart/physiopathology;
Inflammation;
Male;
Myocardial Infarction/prevention & control;
Myocardium/*metabolism;
NF-kappa B/metabolism;
Peroxidase/metabolism;
Pyruvates/*pharmacology;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury/*drug therapy/*metabolism
- From:Yonsei Medical Journal
2010;51(6):838-844
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Ethyl pyruvate has anti-inflammatory properties and protects organs from ischemia/reperfusion (I/R)-induced tissue injury. The aim of this study was to determine whether ethyl pyruvate decreases the inflammatory response after regional I/R injury and whether ethyl pyruvate protects against delayed regional I/R injury in an in vivo rat heart model after a 24 hours reperfusion. MATERIALS AND METHODS: Rats were randomized to receive lactated Ringer's solution or ethyl pyruvate dissolved in Ringer's solution, which was given by intraperitoneal injection 1 hour prior to ischemia. Rats were subjected to 30 min of ischemia followed by reperfusion of the left coronary artery territory. After a 2 hours reperfusion, nuclear factor kappaB, myocardial myeloperoxidase activity, and inflammatory cytokine levels were determined. After the 24 hours reperfusion, the hemodynamic function and myocardial infarct size were evaluated. RESULTS: At 2 hours after I/R injury, ethyl pyruvate attenuated I/R-induced nuclear factor kappaB translocation and reduced myeloperoxidase activity in myocardium. The plasma circulating levels of inflammatory cytokines decreased significantly in the ethyl pyruvate-treated group. At 24 hours after I/R injury, ethyl pyruvate significantly improved cardiac function and reduced infarct size after regional I/R injury. CONCLUSION: Ethyl pyruvate has the ability to inhibit neutrophil activation, inflammatory cytokine release, and nuclear factor kappaB translocation. Ethyl pyruvate is associated with a delayed myocardial protective effect after regional I/R injury in an in vivo rat heart model.