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Effect of lipoxin A4 on myocardial ischemia reperfusion injury following cardiac arrest in a rabbit model.

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.
AuthorsZhiqiao Chen, Zhe Wu, Congxin Huang, Yan Zhao, Yirong Zhou, Xianlong Zhou, Xingxing Lu, Lele Mao, Siying Li
JournalInflammation (Inflammation) Vol. 36 Issue 2 Pg. 468-75 (Apr 2013) ISSN: 1573-2576 [Electronic] United States
PMID23114480 (Publication Type: Journal Article)
Chemical References
  • Anti-Inflammatory Agents, Non-Steroidal
  • Interleukin-1beta
  • Interleukin-6
  • Lipoxins
  • NF-kappa B
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • lipoxin A4
  • Interleukin-10
Topics
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal (pharmacology, therapeutic use)
  • Apoptosis (drug effects)
  • Female
  • Heart Arrest
  • Inflammation (drug therapy)
  • Interleukin-10 (biosynthesis)
  • Interleukin-1beta (biosynthesis)
  • Interleukin-6 (biosynthesis)
  • Lipoxins (pharmacology, therapeutic use)
  • Male
  • Myocardial Reperfusion Injury (drug therapy, metabolism)
  • NF-kappa B (biosynthesis, metabolism)
  • Rabbits
  • Transcription Factor RelA (biosynthesis)
  • Tumor Necrosis Factor-alpha (biosynthesis)

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