Soluble receptor for advanced glycation end-products inhibits myocardial fibrosis of ischemia/reperfusion mice
10.16098/j.issn.0529-1356.2021.05.015
- Author:
Xian-Xian CAO
1
;
Xue-Jie HAN
1
;
Cai-Xia GUO
1
;
Hong-Xia WANG
2
;
Xiang-Jun ZENO
2
Author Information
1. Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University
2. Department of Physiology and Pathophysiology, Capital Medical University
- Publication Type:Journal Article
- Keywords:
Fibrosis;
Immunohistochemistry;
Ischemia/reperfusion;
Mouse;
Soluble receptor for advanced glycation end-products
- From:
Acta Anatomica Sinica
2021;52(5):772-776
- CountryChina
- Language:Chinese
-
Abstract:
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.
