Original Article Protective mechanism of IL-37 in the regulation of Tregs in myocardial ischemia microcirculation reperfusion injury
Int J Clin Exp Pathol
IL-37 is a newly discovered natural inflammatory inhibitor in recent years. The role and mechanism of IL-37 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
... y 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 CK-MB 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 reperfu-sion 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.