IL-33 attenuates cardiac remodeling following myocardial infarction via inhibition of the p38 MAPK and NF-κB pathways.

Abstract The inflammatory response has adverse effects on left ventricular (LV) function and remodeling post-myocardial infarction (MI). Interleukin (IL)-33 is considered to have anti-inflammatory properties. The present study examined whether the suppression of inflammation with IL-33 was able to attenuate LV dysfunction and remodeling post-MI. The MI model was induced and the mice were treated with either saline or recombinant IL-33. Inflammatory mediators, LV functional changes and structural remodeling were evaluated. IL-33 significantly suppressed macrophage infiltration and the production of inflammatory cytokines in the myocardium. IL-33 treatment significantly improved LV function, reduced infarct size and infarct wall thinning. MI-induced activation of the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-κB (NF-κB) pathways was also suppressed. Our data demonstrated that IL-33 suppresses inflammatory responses and improved LV function and remodeling by inhibiting the p38 MAPK and NF-κB pathways. IL-33 may be a potential therapeutic target for heart dysfunction post-MI.