Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model

被引:27
作者
Chen, Zhiqiao [1 ,2 ]
Wu, Zhe [3 ]
Huang, Congxin [4 ]
Zhao, Yan [2 ]
Zhou, Yirong [3 ]
Zhou, Xianlong [3 ]
Lu, Xingxing [3 ]
Mao, Lele [3 ]
Li, Siying [3 ]
机构
[1] Wuhan Univ, Renmin Hosp, Wuhan 430060, Peoples R China
[2] Wuhan Univ, Zhongnan Hosp, Emergency Ctr, Wuhan 430071, Peoples R China
[3] Wuhan Univ, Coll Med, Wuhan 430071, Peoples R China
[4] Wuhan Univ, Renmin Hosp, Dept Cardiol, Wuhan 430060, Peoples R China
关键词
cardiac arrest (CA); cardiopulmonary resuscitation (CPR); ischemia-reperfusion injury (IRI); inflammation; lipoxin A4; TRIGGERED 15-EPI-LIPOXIN A(4); NF-KAPPA-B; INFLAMMATION; DYSFUNCTION; EXPRESSION; APOPTOSIS; CYTOKINES; PROTECTS; RECEPTOR; ANALOG;
D O I
10.1007/s10753-012-9567-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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-1 beta, IL-6, TNF-alpha, and IL-10), NF-kappa B 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-1 beta, IL-6, and TNF-alpha, the values of the infarct ratios, apoptotic index, the level of serum cTnI and NF-kappa B 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-kappa B activation may play an important role.
引用
收藏
页码:468 / 475
页数:8
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