中文摘要：

目的：探讨外源性重组人源性白细胞介素（IL）-37对小鼠心肌缺血再灌注损伤的影响。方法：8~10周雄性c57BL/6小鼠为实验对象,随机分为假手术组、缺血再灌注（I/R）对照组和I/R＋IL-37干预组,每组6只。观察各组小鼠I/R后心肌坏死面积及心功能（24h后）,检测缺血心肌处中性粒细胞募集（MPO）,以及缺血心肌和血清中肿瘤坏死因子α（TNF-α）、IL-1β、IL-6、IL-10、转化生长因子-β（TGF-β）表达（4h后）。结果：与假手术组比较,I/R对照组心功能明显下降,TNF-α、IL-1β和IL-6水平明显增高。IL-37干预组可以明显抑制TNF-α、IL-1β和IL-6表达,增加IL-10与TGF-β水平,减轻MPO,减少心肌坏死面积并改善心功能。结论：IL-37减轻小鼠心肌I/R损伤,可能与抑制MPO、降低促炎因子表达以及上调抗炎因子表达相关。

英文摘要：

Objective： To investigate the effect of IL-37 on myocardial ischemia/reperfusion injury in mice. Method： Sham or I/R operations were performed on male C57BL/6J mice, and I/R mice were randomly divided in- tocontrol group and IL-37 treated group （each group： n= 6）. Then the infarct size and cardiac function were de- tected in 24 hours after reperfusion, the MPO activity was measured as an indicator of neutrophil infiltration in the ischemic myocardium 4 hours after reperfusion, and the expressions of pro-inflammatory cytokines （TNF-α,IL-1β, IL-6） and anti-inflammatory cytokines （IL-10, TGF-β）in heart tissue and serum were measured 4 hours after reperfusion. Result：Compared with sham group, I/R mice showed a decreased cardiac function accompanying with an increased level of pro-inflammatory eytokines （TNF-α, IL-1β, IL-6）. However, compared with I/R control mice, IL-37 treated I/R mice significantly reversed the process as demonstrated by reduced infarct size,improvedcardiac function,suppressed MPO activity and inflammation response balance characteristic with inhibited pro-in- flammatory cytokines （TNF-α, IL-1β, IL-6） and improved anti-inflammatory cytokines （IL-10, TGF-β）. Conclusion：IL-37 plays a protective role against mouse myocardial I/R injury, suppresses the infiltration of neutrophil to- wards ischemic myocardium, which may he associated with the halance of inflammation response.