可溶性晚期糖基化终末产物受体拮抗缺血/再灌注小鼠心肌纤维化

目的 探讨可溶性晚期糖基化终末产物受体（sRAGE）对缺血/再灌注小鼠心脏炎症的影响及其机制。 方法 利用6～8周龄雄性C57BL/6小鼠构建心肌缺血/再灌注损伤模型（左前降支结扎30 min，再灌注2周），随机分为4组，每组5只C57BL/6小鼠。通过心脏超声检测心功能，HE染色观察炎症细胞浸润情况，马松和天狼星红染色检测心肌纤维化，免疫组织化学染色检测半乳糖凝集素3（galecti-3）表达。 结果 与假手术组相比，缺血/再灌注组小鼠的心功能减退，心肌组织间有大量炎症细胞浸润，心肌纤维化面积增加，同时，心脏组织中 galectin-3 的表达增多；而给予外源性sRAGE处理后，小鼠的心功能显著改善，炎症细胞浸润减少，纤维化程度减轻，心脏组织中galecti-3的表达也显著减少。 结论 心肌缺血/再灌注损伤时，sRAGE可能通过抑制galectin-3的表达，减少小鼠心脏炎症细胞浸润，从而减轻心肌纤维化。

Soluble receptor for advanced glycation end-products inhibits myocardial fibrosis of ischemia/reperfusion mice

Objective To investigate the effect of soluble receptor for advanced glycation end-products (sRAGE) on inflammation in myocardial ischemia/reperfusion(I/R) mice and its mechanism. Methods Myocardial I/R injury model was conducted by left anterior descending ligation for 30 minutes and reperfusion for 2 weeks in male C57BL/6 mice aged 6-8 weeks. The mice were randomly divided into four groups with five C57BL/6 mice in each group. The cardiac function was detected by echocardiography, the inflammatory cells infiltration was observed by HE staining, the myocardial fibrosis was detected by Masson and Sirius red staining, the expression of galectin-3 was detected by immunohistochemical staining. Results Compared with the sham group, the cardiac function decreased, the inflammatory cells infiltrated increased among the myocardial tissue, the percentage of myocardial fibrosis area increased, and the expression of galectin-3 increased in I/R groups. After exogenous sRAGE treatment, the cardiac function of mice was significantly improved, the inflammatory cells infiltration decreased, the myocardial fibrosis area decreased, and the expression of galectin-3 decreased as well. Conclusion sRAGE may reduce inflammatory cells infiltration in mice heart by inhibiting the expression of galectin-3, and then alleviating myocardial fibrosis during myocardial ischemia/reperfusion injury.