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Objective To sludy the relationship between rnadvanced glycosylation end products (AGE) and rnprotein kinase C (PKC), and their effects on ranal rnalteration in diabetic rats.rnMethods Insulin or anlinoguanidine was administered rnto diabetic rats. Blood glucose, hermoglobin A1c rn(HbA1c ), glomemlar tissue extracts AGE ( GTErnAGE ), PKC, glomerular basement membrane rnthickness ( GBMT ) and udne protein/creatinine rn(Pr/Cr) ratio in diabetic rats were measured and rnanalysed.rnResults LeveLs of blood glucose, HbA1C and AGE,rnPKC activity, the Pr/Or ratio and GBMT were all rnsignificantly increased ( p values all less than 0.01 ) in rndiabetic rats. Insulin could decrease the formation of rnkbAlc and AGE, and improve PKC activity.rnAminoguanidine had no influecce on PKC activity rn(P>O.05) although it decreased the formation of rnAGE. Botah drugs could de4ay the increase of urine rnPr/Cr ratio and GBMT ( P<0.05 or P< 0.01).rnConclusions Chronic hyperglycemia may lead to an rnincrease of PKC activity. HbAlc and AGE may not rndirectly coritribute to alterations of PKC activity, but the rnincrease of PKC activity could promote the action of rnAGE on GEM thickening. It is important to inhibit the rnformanion of AGE and reduce the PKC activity so as to rnpceveat or delay the development of diabetic rnnephropathy.