|
Objective streptozotocin (Streptozotocin, STZ)-induced diabetic nephropathy rat model to study the kidney of diabetic rats Mangiferin injury in rats and its mechanism. For further development of this drug as well as provide the basis for the treatment of diabetic nephropathy. Methods 40 healthy male weighing 220-250 g Sprague-Dawley (SD) rats were randomly selected from eight normal control group, and the remaining 32 fasted for 12 h, weighed, according to 50 mg / kg body weight intraperitoneal injection of 1% STZ-induced The diabetic rats, blood glucose concentration greater than 16.7 mmol / L in rats were randomly divided into four groups. Grouping by: normal control group, diabetic model group, low dose mangiferin, medium and high dose (15 mg / kg · d, 30 mg / kg · d, 60 mg / kg · d) group. 12 weeks, weighing kidney weight and kidney index calculated using the kit to detect the glucose ,24-h urinary protein, SOD (superoxide dismutase, SOD); hematoxylin - eosin (hemat-oxylin-eosin staining, HE) staining of renal tissue morphological changes; immunohistochemistry and Western blotting (Western Blot) method for the determination of the renal tissue of transforming growth factor-β (transforming growing factor-β, TGF-β), matrix metalloproteinase -2 (matrix metalloproteinases-2, MMP-2) and matrix metalloproteinase inhibitor -2 (tissue inhibitors of matrixmetallo-proteinase-2, TIMP-2) expression. Results ① kidney index calculation results show that: STZ diabetic rats can cause significant damage to kidney function. Model group compared with normal rats, kidney weight and renal hypertrophy index was significantly increased (P lt; 0.01). Mangiferin each group than in model group decreased renal hypertrophy index (P lt; 0.01). ② glucose ,24-h urinary protein and SOD assay Show: model group compared with normal rats, blood glucose and 24-h urine protein was significantly increased (P lt; 0.01), SOD activity was significantly decreased (P lt; 0.01) . Mangiferin each group compared with model group, blood glucose and 24-h urinary protein decreased significantly (P lt; 0.01), SOD activity increased (P lt; 0.05 or P lt; 0.01). ③ HE staining was observed under the microscope after renal tissue morphological changes: Compared with normal group, model group glomerular mesangial matrix, basement membrane thickening, glomerular cells increased glomerular balloon lumen increases Some regional atrophy, sclerosis; Part tubular cell expansion, swelling, mangiferin treatment can suppress the disease in varying degrees. ④ immunohistochemistry and Western Blot method for the determination results: Compared with normal group, model group renal tissue TGF-β and TIMP-2 expression were significantly increased (P lt; 0.01), while the expression of MMP-2 was significantly lower ( P lt; 0.01). Compared with model group, the treatment group Mangiferin renal tissue TGF-β and TIMP-2 expression were significantly reduced (P lt; 0.05 or P lt; 0.01), and MMP-2 expression was significantly increased (P lt; 0.01) . Conclusion ① Mangiferin STZ-induced diabetic rats on kidney function injury in rats. ② Mangiferin can reduce blood sugar, enhance renal cell antioxidant function, reduce the oxygen radical damage to the kidneys, which has a protective effect. ③ Mangiferin on STZ-induced diabetic nephropathy protect its mechanism may regulate kidney basement membrane and extracellular matrix (extra cellular matrix, ECM) metabolism of TGF-β, MMP-2, TIMP-2 related.
|