戎健 邱鸿鑫 汪恕萍 戎健 400042 重庆，第三军医大学大坪医院野战外科研究所内分泌科；邱鸿鑫 汪恕萍 重庆医科大学第一附属医院内分泌科 中华肾脏病杂志 1999 0 15 2


    关键词：糖尿病肾病；非酶促糖基化；蛋白激酶C 期刊 zhszbzz 0 继发性肾小球疾病专题论著 fur -->


    

【摘要 】 目的 探讨糖尿病状态下肾小球晚期糖基化终末产物(AGE)与蛋白激酶C(PKC)的关系及其对肾脏的影响。方法 给予糖尿病大鼠胰岛素和氨基胍治疗，测定血糖，糖化血红蛋白A_1C (HbA₁ C)、肾小球AGE(GTE-AGE)、蛋白激酶C(PKC)、肾小球基底膜厚度(GBMT)和尿Pr/Cr比值。结果 糖尿病大鼠在血糖、HbA_1C 和AGE水平增高的同时，PKC活性、尿Pr/Cr比值和GBMT都显著增加(P值小于0.01)；胰岛素可减少HbA_1C 和AGE形成，恢复PKC活性，氨基胍可减少AGE形成，但对PKC活性无影响。两种药物均可减缓尿Pr/Cr比值和GBMT增加(P<0.01或P<0.05)。结论 慢性高血糖可增高肾小球PKC活性，非酶促糖基化可能未直接参与PKC活性改变，但PKC可加强AGE对肾脏的影响。减少AGE形成，改善PKC活性对糖尿病肾病的防治尤为重要。

Relationship among advanced glycosylation end products,protein kinase C and renal alterations in diabetic rats

RONG Jian,QIU Hongxin,Wang Shuping.Department of Endocrinology, Daping Hospital of Third Military Medical University,Chongqing 400042

【Abstract 】 Objective To explore relationship between advanced glycosylation end products(AGE) and proteinkinase C(PKC),and their effects on renal alterations under diabetes.Methods Insulinor aminoguanidine was administered to diabetic rats.Blood glucose, hemoglobin A_1C (HbA_1C ),glomerular tissue extracts AGE(GTE-AGE), PKC,glomerular basement membrance thickness(GBMT)and urine protein/creatinine(Pr/Cr)ratio in diabetic rats were measured and analysed.Results Levelsof blood glucose, HbA_1C and AGE, PKC activity, the ratio and GBMT were allsignificantly increased(P value all less than 0.01) in diabetic rats. Insulin coulddecrease formation of HbA_1C and AGE, and improve PKC activity.Aminoguamidinehad no influence on PKC activity (P>0.05) although it decreased formation of AGE.Bothof the drugs could delay increase of urine Pr/Cr ratio and GBMT(P<0.05 or P<0.01).Conclusion Chronichyperglycemia may lead to increase of PKC activity.HbA_1C and AGE may notdirectly contribute to alterations of PKC activity . But the increase of PKC activitycould promote the action of AGE on GBM thickening.It is important to inhibit the formationof AGE and reduce the PKC activity so as to prevent or delay the development of diabeticnephropathy.

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