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.
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Authors | Zhiqiao Chen, Zhe Wu, Congxin Huang, Yan Zhao, Yirong Zhou, Xianlong Zhou, Xingxing Lu, Lele Mao, Siying Li |
Journal | Inflammation
(Inflammation)
Vol. 36
Issue 2
Pg. 468-75
(Apr 2013)
ISSN: 1573-2576 [Electronic] United States |
PMID | 23114480
(Publication Type: Journal Article)
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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
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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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