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中国临床药理学与治疗学 ›› 2004, Vol. 9 ›› Issue (9): 1037-1040.

• 研究原著 • 上一篇    下一篇

氨基胍对糖尿病大鼠心脏功能及心肌超微结构的影响

符丽娟, 王洪新, 庞东渤1, 李艳芹2   

  1. 锦州医学院药理学教研室,1附属一院眼科,2电镜室, 锦州121001, 辽宁
  • 收稿日期:2004-07-09 修回日期:2004-08-10 出版日期:2004-09-26 发布日期:2020-11-23
  • 通讯作者: 符丽娟, 女, 硕士, 讲师, 研究方向:心血管药理学。Tel:0416-4561205 E-mail:FLJ1988 @163. com
  • 作者简介:王洪新, 男, 博士, 教授, 硕士生导师, 研究方向:心血管药理学。Tel:0416-4580209 E-mail:jyhxwang @hot mail.com

Influnce of aminoguanidine on myocardial function and ultrastractue in diabetic rats

FU Li-Juan, WANG Hong-Xin, PANG Dong-Bo1, LI Yan-Qin2   

  1. Department of Parmacology,1The First Affiliated Hospital,2Department of Electron Microscope, Jinzhou Medical College, Jinzhou 121001, Liaoning, China
  • Received:2004-07-09 Revised:2004-08-10 Online:2004-09-26 Published:2020-11-23

摘要: 目的: 探讨非酶糖化抑制剂-氨基胍(aminoguanidine, AG)对链尿佐菌素(streptozotocin, STZ)糖尿病大鼠心肌的保护作用, 为糖尿病心肌病的防治提供参考。方法: 建立STZ 糖尿病大鼠模型, 随机分为对照组、糖尿病组和氨基胍治疗组,AG 剂量为150 mg·kg-1·d-1。12 周时测定大鼠血清果糖胺含量、心脏重量指数、左室内压最大上升和下降率(±dp/dtmax)值, 电镜观察心肌超微结构, 测量心肌毛细血管基底膜厚度。结果: 糖尿病组大鼠血清果糖胺含量、心脏重量指数明显增高,±dp/d tmax 降低;超微结构显示心肌肌原纤维排列紊乱, 线粒体肿胀变性,间质胶原增生, 微血管内皮细胞肿胀、基底膜明显增厚。氨基胍治疗组血清果糖胺含量降低、心脏重量指数明显下降、±dp/d tmax 值上升, 微血管基底膜增厚减轻, 间质胶原减少, 心肌细胞超微结构异常减轻。结论: 糖尿病时存在心脏功能异常、心肌肥厚和超微结构的改变, 早期应用AG 在一定程度上可阻抑糖尿病心肌病变的发展。

关键词: 氨基胍, 非酶糖化, 糖尿病大鼠, 心肌病

Abstract: AIM: To explore the protective effects of the nonenzymation glycosylation inhibitor-aminoguanidine (AG)on the cardiac function and ultrastructure in diabetes-induced rats.METHODS: Sprague-Dawley rats were randomly divided into control group, sreptozotocin(STZ)-induced diabetic group and aminoguanidine treated diabetic group (150 mg·kg-1·d-1 water given after diabetes induced).The serum fructosamine content levels and the cardiac mass index and some related parameters were determined at 12 weeks.RESULTS: The serum fructosamine content levels and the cardiac mass were higher than that in the control group. The value of±dp/dtmax tite was decreased in diabetic group at 12 weeks compared with the control group. Electron microscopic morphometry of heart samples revealed typical diabetic alterations consisting in a focal loss, disorganization of myofibril, mitochondril swelling, and lysis of cistae. In AG treated group, The serum fructosamine content levels and the cardiac mass decreased, the value of±dp/dtmax was increased markedly compared with diabetic rats. Microvascular membrane, proliferation of the collegen in the extracellular matrix and nyocardial ultrastructure were better than diabetes.CONCLUSION: There are changes of myocardial function, ultrastractue abnormalities and ventricular hypertropfhy in diabetic rats. AG can inhibit the progress of diabetic cardiomyopathy.

Key words: aminoguanidine, nonenzymation glycosylation, diabetic rat, cardiomyopathy

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