糖基化终产物在糖尿病大鼠心肌病变中的作用

目的观察糖尿病心肌病变过程中心肌组织糖基化终产物（advanced glycosylation endproducts，AGEs）的变化，探讨AGEs对糖尿病大鼠心肌的影响。方法建立糖尿病大鼠模型，随机分为对照组（CON）、糖尿病组（DM）和氨基胍治疗组（AG），饲养12周。分别测定各组大鼠血糖、血清LDH、CK活性、心脏重量指数、血清果糖胺（FMN）及AGEs含量、电镜观察心肌超微结构。结果DM组大鼠血糖、血清LDH、CK活性、心脏重量指数、血清果糖胺（FMN）及AGEs含量明显高于CON组。超微结构显示心肌肌原纤维排列紊乱，间质胶原增生，微血管基底膜增厚，管腔狭窄。AG组大鼠血清LDH、CK活性、心脏重量指数、血清果糖胺（FMN）及AGEs含量明显降低。微血管基底膜增厚减轻，问质胶原减少，心肌细胞超微结构异常减轻。结论AGEs在糖尿病心肌改变的发生中起重要作用。

The Effect of Advanced Glycosylation Endproducts on Diabetes-induced Cardiomyopathy

Objective To observe the changes of advanced glycosylation endproducts of myocardium in early peiroid of diabetes-induced cardiac disease and explore the effect of advanced glycosylation endproducts on diabetes-induced cardiomyopathy. Methods Sprague-Dawley Rats were randomly divided into control group, Streptozotocin（STZ）-induced diabetic group and aminoguanidine treated diabetic group. The cardiac mass index , blood glucose, serum l-lactate dehydrogenase（LDH）, creatine kinase（CK） and serum fructosamine（FMN） were assayed at 12 weeks. We also measured myocardial tissue AGEs and observed myocardial ultrastructure. Results The cardiac mass index, the levels of LDH, CK, FMN and myocardial tissue AGEs were higher than those of the control. Electron microscopic morphometry of heart samples revealed typical diabetic alterations consisting of focal loss, disorder of myofibril, hyperplasia of interstitial collagen, microvascular membrane thickening and lumen stenosis. In AG treated group, the serum fructosamine levels, myocardial tissue AGEs and the cardiac mass index decreased, Microvascular membrane thickening and lumen stenosis, proliferation of the collegen in the extracellular matrix and myocardial ultrastucture were relieved. Condusion AGEs may play a role in the pathogenesis of diabetic cardiaomyopathy, the administration of aminoguanidine could partially reverse the change of diabetic heart.