摘要
目的 探讨糖尿病状态下肾小球蛋白激酶C(PKC)与肾脏改变的关系。方法 对链脲菌素诱发的糖尿病大鼠喂养 2 8周 ,同时对部分糖尿病大鼠进行胰岛素治疗。测定糖尿病大鼠血糖、糖化血红蛋白A1c(HbA1c)、PKC活性、肾小球基底膜厚度 (GB MT)和尿蛋白质 肌酐 (Pr Cr)比值 ,并与正常对照组比较。结果 糖尿病大鼠在血糖水平和HbA1c含量增高的同时 ,PKC活性、GB MT和尿Pr Cr比值都显著增加 (P <0 .0 1 ) ;PKC活性与血糖相关 (P <0 .0 1 ) ,而与HbA1c无显著相关性 (P >0 .0 5 ) ,胰岛素治疗可通过降低血糖水平来减少HbA1c形成、改善PKC活性 ,从而减缓GBMT增加 ,减少尿蛋白排出。结论 高血糖慢性刺激可引起肾小球PKC活性增高 ,非酶促糖基化可能未直接参与PKC活性改变 。
Objective To evaluate the relationship between glomerular protein kinase C (PKC) and renal alterations under diabetic state. Methods The streptozotocin induced diabetic rats were fed for 28 weeks. Insulin was administered to some of them after the onset of diabetes. Then blood glucose, hemoglobin Alc (HbAlc), glomerular PKC activity, glomerular basement membrane thickness (GBMT) and urine protein/creatinine (Pr/Cr) ratio in diabetic rats were measured and compared with those in the control. Results The levels of blood glucose, HbAlc content, PKC activity and GBMT were significantly higher in diabetic rats than those in the control ( P <0.01). Insulin treatment could decrease the levels of blood glucose, reduce HbAlc content, ameliorate PKC activity and delay the thickening of glomerular basement membrance (GBM). Conclusion Chronic stimulation of hyperglycemia may increase PKC activity. Nonenzymatic glycosylation may not directly contribute to increasing PKC activity. Long term increase of PKC activity may enhance the development and progression of diabetic nephropathy.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2001年第1期78-80,共3页
Journal of Third Military Medical University
关键词
糖尿病肾病
肾小球基底膜
非酶促糖基化
蛋白激酶C
diabetic nephropathy
glomerular basement membrance
nonenzymatic glycosylation
protein kinase C
