American Journal of BioMedicine
Received October 12, 2019; Accepted December 11, 2019; Published January 19, 2020
AJBM 2020;8 (1): 31-48
http://dx.doi.org/10.18081/2333-5106/020/21
Ling Ogiku; Runqiu Fujii; Song Xiao; Liu Xuehao
Abstract
Myocardial injury caused by global ischemia/reperfusion is a complicated pathophysiological course, in which inflammation is thought to play an important role. Endothelial dysfunction plays a critical role in the pathogenesis of reperfusion injury in the myocardium. This role stems from the close proximity of the endothelium to neutrophils and other inflammatory cell types at the vascular interface during the critical early phase as well as the later phase of reperfusion. IL-17A is a cytokine expressed by a variety of cells in response to inflammatory cytokines that are released following tissue injury and/or inflammation. IL-17A induces epithelial cells to secrete neutrophil chemoattractants. The cytokine IL-23, which can be produced by epithelial cells, plays an important role in IL-17A production. Global myocardial injury induced by abdominal heart transplant model in IL-17A deficient (Il17a-/-), IL-23R deficient (Il23r-/-) and WT mice. Our data showed that cTn-I, neutrophil accumulation MCP-1 and ICAM-1 were significantly less in both Il17a-/- mice and Il23r/- mice than in WT controls. These two pathways may become possible therapeutic targets for the treatment of global ischemia induced myocardial injury.
Keywords: Myocardial injury; Global ischemia/reperfusion; IL-17A; IL-23
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