摘要
To study the relationship between advanced glycosylation end products (AGE) and protein kinase C (PKC), and their effects on renal alteration in diabetic rats Methods Insulin or aminoguanidine was administered to diabetic rats Blood glucose, hemoglobin A 1C (HbA 1C ), glomerular tissue extracts AGE (GTE AGE), PKC, glomerular basement membrane thickness (GBMT) and urine protein/creatinine (Pr/Cr) ratio in diabetic rats were measured and analysed Results Levels of blood glucose, HbA 1C and AGE, PKC activity, the Pr/Cr ratio and GBMT were all significantly increased ( P values all less than 0 01) in diabetic rats Insulin could decrease the formation of HbA 1C and AGE, and improve PKC activity Aminoguanidine had no influence on PKC activity ( P >0 05) although it decreased the formation of AGE Both drugs could delay the increase of urine Pr/Cr ratio and GBMT ( P <0 05 or P <0 01) Conclusions Chronic hyperglycemia may lead to an increase of PKC activity HbA 1C and AGE may not directly contribute to alterations of PKC activity, but the increase of PKC activity could promote the action of AGE on GBM thickening It is important to inhibit the formation of AGE and reduce the PKC activity so as to prevent or delay the development of diabetic nephropathy
To study the relationship between advanced glycosylation end products (AGE) and protein kinase C (PKC), and their effects on renal alteration in diabetic rats Methods Insulin or aminoguanidine was administered to diabetic rats Blood glucose, hemoglobin A 1C (HbA 1C ), glomerular tissue extracts AGE (GTE AGE), PKC, glomerular basement membrane thickness (GBMT) and urine protein/creatinine (Pr/Cr) ratio in diabetic rats were measured and analysed Results Levels of blood glucose, HbA 1C and AGE, PKC activity, the Pr/Cr ratio and GBMT were all significantly increased ( P values all less than 0 01) in diabetic rats Insulin could decrease the formation of HbA 1C and AGE, and improve PKC activity Aminoguanidine had no influence on PKC activity ( P >0 05) although it decreased the formation of AGE Both drugs could delay the increase of urine Pr/Cr ratio and GBMT ( P <0 05 or P <0 01) Conclusions Chronic hyperglycemia may lead to an increase of PKC activity HbA 1C and AGE may not directly contribute to alterations of PKC activity, but the increase of PKC activity could promote the action of AGE on GBM thickening It is important to inhibit the formation of AGE and reduce the PKC activity so as to prevent or delay the development of diabetic nephropathy
