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.