Interleukin-27 attenuates myocardial injury after ischemia-reperfusion through down-regulation of inflammatory response



The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial injury and inflammatory response is an important process during the pathogenesis of myocardial I/R injury. IL-27, this cytokine is mainly produced by cells of myeloid origin such as monocytes, macrophages, dendritic cells, and microglial cells, in response to stimuli acting through Toll-like receptors. The objective of present study is to assess whether IL-27 can improve ventricular function after myocardial ischemia by down-regulation of inflammatory response. The results demonstrated that the IL-27 markedly attenuated Left Ventricular Function (LVF) in mice model, and reduced plasma level of cTn-I as marker of cardiac injury. Moreover, the IL-27 was associated with up-regulation in both chemokine and cytokines expression following I/R, through down-regulation of activation of JAK/STAT pathway.

Keywords: IL-27; proinflammatory cytokines; myocardial I/R injury

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Research Article
American Journal of BioMedicine Volume 7, Issue 2, pages 104-117
Received October 30, 2018; accepted January 21, 2019; published February 25, 2019

How to cite this article
Mai HN, Lee YS, Chang EH, Lee S. Interleukin-27 attenuates myocardial injury after ischemia-reperfusion through down-regulation of inflammatory response. American Journal of BioMedicine 2019;7(2):104-117.

Case report outline
1. Abstract
2. Keywords
3. Introduction
4. Methods
5. Results
6. Discussion
7. References

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