Protective mechanism of IL-37 in the regulation of Tregs in myocardial ischemia microcirculation reperfusion injury

IL-37 is a newly discovered natural inflammatory inhibitor in recent years. The role and mechanism of IL37 in the inflammatory reaction of atherosclerosis in patients with coronary artery disease may be related to the abnormal blood lipid and regulatory T cells (Tregs). But the effect of IL-37 on myocardial ischemia reperfusion injury and its mechanism are still not clear. Therefore, this study will do the protection mechanism of IL-37 in myocardial infarction microcirculation reperfusion injury by regulating Treg. Rat myocardial microcirculatory reperfusion injury model was established. Rats were randomly divided into three groups, A. normal group; B. model group; C. IL-37 administration group. Serum lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB), superoxide dismutase (SOD) in the myocardial tissue live, content of MDA, NOS activity, NO content, Tregs cell ratio, Foxp3 and CTLA-4 mRNA expression levels, protein in the spleen tissue expression level were examined. Serum LDH and CKMB were lower in IL-37 group than that in model group. SOD activity, NOS activity and NO increased in myocardium while MDA decreased (LDH and CK-MB: P<0.05, SOD, MDA, NOS and NO: P<0.01). Tregs cells in IL-37 group were increased (P<0.05). FoxP3 and CTLA-4 was lower in the model. If we provided the IL-37, FoxP3 and CTLA-4 expression increased. In Tregs cells FoxP3 and CTLA-4 mRNA expression were decreased P<0.01). IL-37 group was versed model group, IL-6 and TGF-α decreased. IL-37 has protective effect on myocardial infarction microcirculation reperfusion injury, decrease serum LDH and CK-MB values, increase SOD activity, NOS activity, NO content, decrease MDA, and its mechanism may be to promote Tregs cells, inhibit inflammatory reaction, and the expression of CTLA-4 and FoxP3.