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Introduction: In diabetes mellitus the increase of AgII (Angiotensin II), IGF-1(insulin like growth factor-1) and growth hormone induce kidney lesions especially changes in content and thickness of GBM and widening and fusion of podocyte pedicles. In this research for the first time the combination of Losartan (AT1 receptor blocker) and Octreotide (Somatostatin analogue) were used in order to prevent glomerular epithelial lesions.
Materials & Methods: In this experimental study 15 male rats (2 months age) were uninephrectomised from left flank and divided in 5 groups (3 per group). 7 days later diabetes was induced in 2th, 3th, 4th and 5th group by Alloxan (120mg/kg) subcutaneously. 5 days after diabetes induction, the third group received Losartan (5mg/kg/day) orally, 4th group Octretide (10 ŭg/day) subcutaneously and 5th group both two drugs with the mentioned doses for 8 weeks. The 2th group was served as diabetic non treatment group. Kidneys of all groups were fixed by perfusion technique. After second fixation of 1 mm3 cortex parts in Osmium Tetroxide, they were processed in TAAB812 resin for embedding. Thin sections (600 nm thickness) were prepared and investigated by transmission electron microscope qualitatively.
Results: Losartan inhibited fusion and thickening of podocyte pedicles but in some cases couldn,t maintain the 3 layer form of GBM. Octreotide had little effect on inhibition of fusion and thickening of podocyte pedicles and no effect in 3 layer form maintaining of GBM. Combined therapy inhibited fusion and thickening of podocyte pedicles and maintained 3 layer form of GBM but in some cases the lamina rara near endothelium was not seen.
Conclusion: Octreotide have little effect on prevention of glomerular epithelium lesions. However Losartan could prevent glomerular epithelium lesions well, but combined drug therapy showed better results comparing Losartan.

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Background: Diabetic nephropathy is one of the most common causes of end stage renal diseases. The aim of this study was to evaluate the antioxidant, anti-diabetic, and anti-inflammatory roles of rosmarinic acid in inhibition of diabetic nephropathy. Materials and Methods:In this experimental study, 40 male rats were uninephrectomized from the left flank. The rats were randomly divided into four groups of ten: Group1 (control), group 2 (control) including untreated diabetic rats, and groups 3 and 4 (treatment groups) that received rosmarinic acid 100 and 200 mg/kg, respectively. Diabetes was induced in groups 2, 3, and 4 by subcutaneous injection of alloxan. After 8 weeks, serum malondialdehyde was measured. Kidney paraffin sections were prepared and stained by periodic acid Schiff method. Glomerular, intraglomerular mesangial, and glomerular capillary volumes were estimated by stereological methods. Data were analyzed by SPSS 13 software and Man-Whitney nonparametric test. Results: The level of serum malondialdehyde in treatment groups was maintained at the level of control group. Glomerular hypertrophy, mesangial expansion, and reduction of glomerular capillary volume in groups treated by rosmarinic acid were significantly inhibited compared with the untreated diabetic group, but the levels of these variables were significantly different from that of the control group. Conclusion: Rosmarinic acid significantly ameliorates glomerular hypertrophy, mesangial expansion, and glomerullar capillary volume in diabetic rats.