非酶糖化抑制剂对糖尿病大鼠心肌细胞凋亡作用的研究

目的: 观察非酶糖化抑制剂-氨基胍(AG) 对糖尿病大鼠心肌细胞凋亡的影响。方法: 54 只SD大鼠分为12 周对照组(8 只), 24 周对照组(10 只);糖尿病12 周组(8 只), 糖尿病24 周组(10 只);AG治疗12 周组(8 只), AG 治疗24 周组(10 只), 观察糖尿病大鼠心肌病变过程中(12 周及24 周) 心脏肥厚、心功能指标及心肌细胞凋亡的改变。结果: 链尿佐菌素(STZ) 诱导的糖尿病大鼠12 周时出现心功能异常并可见凋亡的心肌细胞, 随心衰的加重, 24 周时凋亡细胞数目明显增多。透射电镜检查, 发现糖尿病大鼠左室心肌组织中可见凋亡的心肌细胞(具有凋亡形态学特征) 。AG 治疗组大鼠心功能和心肌超微结构明显改善, 心肌细胞凋亡数目减少。结论: 心肌细胞凋亡在糖尿病心肌病发生发展过程中起着重要作用, AG 可有效减少心肌细胞凋亡, 改善心肌病理形态学异常。

Research of nonenzymation glyscation inhibitor on cardiac myocyte apoptosis in diabetic rats with heart failure

AIM: To observe the effects of nonenzymation glyscation inhibitor-aminoguanidine on cardiac myocyte apoptosis in diabetic rats with heart failure. METHODS: SD rats were randomly divided into six groups:12-week control group (n=8), 12-week diabetic group which induced by streptozotocin (STZ) (n=8), 12-week AG treated group (n=8), 24-week control group (n=10), 24-week diabetic group (n=10), and 24-week AG treated group (n=10).Heart function and ventricular remodeling parameters were observed at 12 and 24 weeks.The dynamic changes of cardiac myocyte in left venticle of diabetic rats were observed by situ TdT-mediated dUTP nick end labeling (TUNEL) and transmission electron microscope.RESULTS: Abnormal heart function and myocyte apoptosis were observed at 12-week and aggravated at 24-week in diabetic rats.Electron microscopic features of cardiocyte apoptosis were identified in left ventricle.The heart function improved and the number of apoptosis myocytes decreased in AG group.CONCLUSION: Myocyte apoptosis plays an important role in the development of heart failure in diabetic rats.AG can improve the heart function and inhibit myocyte apoptosis.