IL-10 Inhibits Inflammation and Attenuates Left Ventricular Remodeling After Myocardial Infarction via Activation of STAT3 and Suppression of HuR

摘要: Persistent inflammatory response has adverse effects on left ventricular (LV) function and remodeling following acute myocardial infarction. We hypothesized that suppression of inflammation with interleukin (IL)-10 treatment attenuates LV dysfunction after After the induction infarction, mice were treated either saline or recombinant IL-10, functional structural changes evaluated. IL-10 significantly suppressed infiltration cells expression proinflammatory cytokines in myocardium. These associated IL-10-mediated inhibition p38 mitogen-activated protein kinase activation repression cytokine mRNA-stabilizing HuR. improved functions, reduced infarct size, attenuated wall thinning. Myocardial infarction-induced increase matrix metalloproteinase (MMP)-9 activity was increased fibrosis, whereas both MMP-9 fibrosis. Small interfering RNA knockdown HuR mimicked reduction NIH3T3 cells. Moreover, capillary density infarcted myocardium which enhanced STAT3 phosphorylation. Taken together, our studies demonstrate suppresses contributes to by inhibiting fibrosis via HuR/MMP-9 enhancing through STAT3.