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一结果：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 inhi bi tor-aminoguanidine on cardiac myocyte apoptosis in diabetic rats with heart fai lure. METHODS: SD rats were randomly divided into six groups: 1 2-week co ntrol group (n=8), 12-week diabetic group which induced by stre ptozotocin (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). He art function and ventricular remodeling parameters were observed at 12 and 24 we eks. The dynamic changes of cardiac myocyte in left venticle of diabetic rats we re observed by situ TdT-mediated dUTP nick end labeling (TUNEL) and transmissio n electron microscope. RESULTS: Abnormal heart function and myoc yte apoptosis were observed at 12-week and aggravated at 24-week in diabetic r ats. Electron microscopic features of cardiocyte apoptosis were identified in le ft ventricle. The heart function improved and the number of apoptosis myocytes d ecreased in AG group. CONCLUSION: Myocyte apoptosis plays an imp ortant role in the development of heart failure in diabetic rats. AG can improve the heart function and inhibit myocyte apoptosis.