Abstract
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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