IL-37 protects myocardial ischemia reperfusion injury in mice through mediating inflammation response

Abstract

Objective: To investigate the mechanism of IL-37 in alleviating myocardial ischemia reperfusion injury by regulating inflammatory response balance. Method: 30 Wistar male mice were randomly and equally assigned into Sham group (Sham operation), IL-37 intervention group (I/R plus IL-37 intervention, short for experimental group) and control intervention group (I/R+normal saline, short for control group), respectively. Sham operation or myocardial Ischemia Reperfusion (I/R) model were performed in Wistar male mice. Mice in experimental group received human recombined IL-37 intervention. The infarction area and cardiac function were examined. The expression of TNF-α, IL-1β, IL-6 and TGF-β in serum and myocardial infarction border zone were measured. MPO activity was examined as an indicator of neutrophil recruitment. Result: Compared with control group, I/R infarction area of mice in experimental group were significantly decreased (P<0.01), while EF and FS was increased remarkably (P<0.05). Compared with Sham group, the level of TNF-α, IL-1β, IL-6 and TGF-β in serum and myocardial infarction border zone was increased both in control and experimental group (P<0.01), with significantly increased MPO activity (P<0.01). Moreover, the level of TNF-α, IL-1β, IL-6 and MPO in serum and myocardial infarction border zone in experimental group was significantly lower than that in control group (P<0.01). However, the TGF-β level was higher in experimental group than that in control group (P<0.01). Conclusions: IL-37 could decrease I/R infarction area and improve cardiac function after myocardial ischemia reperfusion injury. The protective effect of IL-37 against I/R injury might be associated with down-regulating the secretion of proinflammatory factors, inhibiting MPO expression and up-regulating the secretion of anti-inflammatory cytokines.