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Oxidative Medicine and Cellular Longevity
Volume 2018 (2018), Article ID 5216383, 11 pages
Research Article

Edaravone Improves Septic Cardiac Function by Inducing an HIF-1α/HO-1 Pathway

1Department of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China
2Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China

Correspondence should be addressed to Feng Xiao; nc.ude.usc@uscgnefoaix

Received 28 September 2017; Revised 20 December 2017; Accepted 6 February 2018; Published 22 March 2018

Academic Editor: Raquel Rodrigues-Díez

Copyright © 2018 Chao He et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Septic myocardial dysfunction remains prevalent and raises mortality rate in patients with sepsis. During sepsis, tissues undergo tremendous oxidative stress which contributes critically to organ dysfunction. Edaravone, a potent radical scavenger, has been proved beneficial in ischemic injuries involving hypoxia-inducible factor- (HIF-) 1, a key regulator of a prominent antioxidative protein heme oxygenase- (HO-) 1. However, its effect in septic myocardial dysfunction remains unclarified. We hypothesized that edaravone may prevent septic myocardial dysfunction by inducing the HIF-1/HO-1 pathway. Rats were subjected to cecal ligation and puncture (CLP) with or without edaravone infusion at three doses (50, 100, or 200 mg/kg, resp.) before CLP and intraperitoneal injection of the HIF-1α antagonist, ME (15 mg/kg), after CLP. After CLP, rats had cardiac dysfunction, which was associated with deformed myocardium, augmented lipid peroxidation, and increased myocardial apoptosis and inflammation, along with decreased activities of catalase, HIF-1α, and HO-1 in the myocardium. Edaravone pretreatment dose-dependently reversed the changes, of which high dose most effectively improved cardiac function and survival rate of septic rats. However, inhibition of HIF-1α by ME demolished the beneficial effects of edaravone at high dose, reducing the survival rate of the septic rats without treatments. Taken together, edaravone, by inducing the HIF-1α/HO-1 pathway, suppressed oxidative stress and protected the heart against septic myocardial injury and dysfunction.