氨基胍对糖尿病大鼠非酶糖化和细胞凋亡的影响

目的观察氨基胍对2型糖尿病大鼠肾脏晚期糖基化终末产物（AGEs）和细胞凋亡的影响。方法利用高糖高脂饮食及注射小剂量的链脲佐菌素（STZ）建立2型糖尿病大鼠模型,随机分为糖尿病组、氨基胍组,并设对照组,分别于16周观察大鼠肾脏形态结构、肾脏凋亡相关蛋白Bcl-2和Bax表达和肾皮质AGEs含量。结果电镜下见糖尿病组肾脏小管上皮细胞呈典型的凋亡改变,氨基胍组细胞凋亡明显减轻。免疫组化显示,糖尿病组肾小管上皮细胞中Bcl-2、Bax表达较对照组增多,氨基胍组Bcl-2蛋白表达较糖尿病组增多,Bax蛋白表达减少。氨基胍组大鼠肾皮质AGEs含量较糖尿病组明显减少。结论氨基胍可通过降低糖尿病肾皮质AGEs含量调节凋亡相关蛋白Bcl-2和Bax的表达,抑制肾脏细胞凋亡。

The effects of aminoguanidine on tissue nonenzymatic glycation and kidney apoptosis in diabetic rats

Objective To explore the effects of aminoguanidine on the advanced glycosylation end products and apoptosis in the kidney of diebetic rat.Methods The model was established by long term fat enriched and high energy diet ,lower dose of streptozotocin treated rats.Wistar rats were randomly divided into two groups：induced diabetic rats（DM group）,aminoguanidine treated diabetic rats（AG group） ,established the control group rats（CON group） at the same time.Aminoguanidine was administered to diabetic rats for 16 weeks.Contents of AGEs in cortex of kidney were measured and analysed.Examined morphological changes of the kidney of diabetic rats treated with aminoguanidine.Investigated the signal protein expression relating apoptosis of Bcl-2 and Bax.Results Under transmission electronic microscope,typical morphological changes of apoptosis were observed among renal tubular epithelial cells in DM groups.Immuno-histochemistry showed：in DM groups,the expression of Bcl-2、Bax increased significantly.By AG group treatment,the number of apoptotic cell and the level of expression of Bax decreased,the expression of Bcl-2 in increased.Compared with CON group,contents of AGEs in cortex of kidney of DM group significantly increased.By AG group treatment contents of AGEs decreased.Conclusion Aminoguanidine can reduce contents of AGEs in cortex of kidney of diabetic rat and regulate the apoptosis by promoting the expression of Bcl-2 and decreasing the expression of Bax.