Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model
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Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model Zhiqiao Chen,1,2 Zhe Wu,3 Congxin Huang,4,5 Yan Zhao,2,5 Yirong Zhou,3 Xianlong Zhou,3 Xingxing Lu,3 Lele Mao,3 and Siying Li3
Abstract—In the present study, we investigated the effect of lipoxin A4 on myocardial ischemia– reperfusion injury (IRI) following cardiac arrest (CA) in a rabbit model. Lipoxin A4 is a metabolite of arachidonic acid in the eicosanoid, it is called “brake signal” for its anti-inflammatory activity. Some inflammatory factors (IL-1β, IL-6, TNF-α, and IL-10), NF-κB p65, infarct ratios, apoptotic index, cardiac troponin I (cTnI), hemodynamic and myocardial structures were measured or observed in different groups. Lipoxin A4 inhibits the expression of IL-1β, IL-6, and TNF-α, the values of the infarct ratios, apoptotic index, the level of serum cTnI and NF-κB p65. Meanwhile, it improves the expression of IL-10, hemodynamic, myocardial structure, and function. These indicate that lipoxin A4 mitigates postresuscitation myocardial IRI in which anti-inflammation and suppression of NF-κB activation may play an important role. KEY WORDS: cardiac arrest (CA); cardiopulmonary resuscitation (CPR); ischemia–reperfusion injury (IRI); inflammation; lipoxin A4.
cause multiple organ failure, which is a major cause of poor prognosis [2–4]. It is reasonable to speculate that promoting the regression of inflammation is important to advanced life support following CPR. It has been demonstrated that liopxin A4 negatively regulates inflammatory cells, express some inflammationrelated genes, and has been shown to increase the expression of some anti-inflammatory factors including IL-2, IL-4, and IL-10 [5, 6]. Thus, lipoxin A4 has been considered as “brake signal” in the inflammatory response due to anti-inflammatory activity [7]. To date, the protective effect via anti-inflammation of lipoxin A4 has been confirmed in cerebral IRI and other organs [8–15]. However, to our knowledge, the effect of lipoxin A4 on myocardial IRI following cardiac arrest has not yet been reported. In our study, we investigated whether lipoxin A4 has a protective effect on myocardial IRI following cardiac arrest in a rabbit model of CPR.
INTRODUCTION Although considerable progress in cardiopulmonary resuscitation (CPR) has improved the restoration of spontaneous circulation (ROSC) in cardiac arrest (CA) victims, unfortunately, only 8–25 % of the patients are discharged alive from hospital [1]. Many studies have demonstrated that the body experiences ischemia–reperfusion injury (IRI) after CPR due to cardiac arrest. Under this condition, the endothelial system and inflammatory cascade were activated resulting in systemic inflammatory response syndrome; further aggravation of this condition may 1
Renmin Hospital of Wuhan University, 238 JieFang Road, Wuhan, 430060, People’s Republic of China 2 Emergency Center, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, People’s Republic of China 3 Medical College of Wuhan University, 115 D
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