To explore the therapeutic effect and mechanism of Bushen Huoxue Xiezhuo Decoction (BHXD) in treating minute lesion nephropathy (MLN) in rats. Methods: The MLN model rats established by a single intravenous injection of Adriamycin were divided into the model and the BHXD groups, and a normal group was set up for control. The effects of treatment on renal function, hemorrheologic parameters, renal tissue transforming growth factor β1 (TGF-β1) expression and poly-anion sites on glomerular basement membrane were observed dynamically. Results: After treatment, all the parameters between the BHXD group and the model group were significantly different respectively, morphological observation also showed the pathological changes in the BHXD group were milder than those in the model group. Conclusion: BHXD treatment could markedly improve the renal function, alleviate blood hypercoagulability and hyperviscosity, protect the anion barrier and delay the progression of glomerular fibrosis and sclerosis.

Objective To sludy the relationship between advanced glycosylation end products (AGE) and protein kinase C (PKC), and their effects on ranal alteration in diabetic rats.Methods Insulin or anlinoguanidine was administered to diabetic rats. Blood glucose, hermoglobin A1c (HbA1c ), glomemlar tissue extracts AGE ( GTEAGE ), PKC, glomerular basement membrane thickness ( GBMT ) and udne protein/creatinine (Pr/Cr) ratio in diabetic rats were measured and analysed.Results LeveLs of blood glucose, HbA1C and AGE,PKC activity, the Pr/Or ratio and GBMT were all significantly increased ( p values all less than 0.01 ) in diabetic rats. Insulin could decrease the formation of kbAlc and AGE, and improve PKC activity.Aminoguanidine had no influecce on PKC activity (P>O.05) although it decreased the formation of AGE. Botah drugs could de4ay 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. HbAlc and AGE may not directly coritribute to alterations of PKC activity, but the increase of PKC activity could promote the action of AGE on GEM thickening. It is important to inhibit the formanion of AGE and reduce the PKC activity so as to pceveat or delay the development of diabetic nephropathy.