Galectin-3在缺血性心功能不全家兔心室重构中的作用

摘要

AIM: To investigate the relationship between galectin-3 (Gal-3) and myocardial fibrosis, and to clarify the role of Gal-3 in ventricular remodeling in rabbits with ischemic cardiac insufficiency.METHODS: A rabbit model of ischemic cardiac insufficiency was established by ligation of the anterior descending branch of the coronary artery.The 20 rabbits were randomly divided into sham operation group and cardiac insufficiency group by random number table method.After 4 weeks of coronary artery ligation, the cardiac function was measured by cardiac echocardiogram.Real-time PCR and Western blot were used to detect the expression of Gal-3, type I collagen and type III collagen at mRNA and protein levels in the myocardium.The serum Gal-3 contents were measured by ELISA.HE staining and Masson staining were used to observe the degree of fibrosis development in myocardial tissues after infarction.RESULTS: Compared with sham operation group, the mRNA expression of Gal-3 in cardiac insufficiency group was significantly increased.At the same time, type I collagen, type III collagen and collagen type I/III ratio were also increased significantly.The protein contents of Gal-3, type I collagen and type III collagen were increased significantly.The serum Gal-3 levels were significantly increased.The pathological changes were observed in cardiac insufficiency group as the myocardial cell morphological disorder and marked hyperplasia of fibrous tissue were seen.CONCLUSION: Gal-3 aggravates myocardial fibrosis in rabbits with ischemic cardiac insufficiency, and promotes the ventricular remodeling and the occurrence of heart failure.%目的: 探讨半乳糖凝集素3(galectin-3,Gal-3)与心肌纤维化的关系,明确Gal-3在缺血性心功能不全家兔心室重构中的作用.方法: 采用结扎冠状动脉前降支的方法制作缺血性心功能障碍家兔模型.利用随机数字表法将20 只家兔随机分为假手术组和心功能不全组.造模成功4周后采用心脏超声测定心功能;real-time PCR和Western blot方法分别检测心肌中Gal-3、Ⅰ型胶原和Ⅲ型胶原的 mRNA 表达和蛋白含量;ELISA法检测家兔血清中Gal-3水平;采用HE染色和Masson染色法检测家兔梗死区心肌组织的纤维化程度.结果: 与假手术组相比,心功能不全组梗死区心肌组织Gal-3的mRNA和蛋白表达明显增加,与此同时Ⅰ型胶原和Ⅲ型胶原的mRNA和蛋白表达也明显增加;血清Gal-3水平明显上升;病理学观察可见心功能不全组的心肌细胞形态不一、排列紊乱,纤维组织明显增生.结论: Gal-3加重了缺血性心功能不全家兔的心肌纤维化,促进了心室重构和心衰的发生.