| ObjectiveDiabetes was induced by intraperitoneal injection with streptozotocin (STZ) in rats. Effects of mangiferin and therapeutic mechanism were investigated in diabetic nephropathy rats, in order to develop of this drug and provide experiment foundation for clinical therapy of diabetic nephropathy.MethodsNormal control group were randomly selected eight rats from 40 healthy male Sprague-Dawley (SD) rats with weighing 220-250 grams. The remaining 32 SD rats were fasting for 12 hours and weighed, then were induced 1% STZ by intraperitoneal injection, according to 50 mg/kg body weighten. If blood glucose of the rats were more than 16.7 mmol/L, the rats were randomly divided into 4 groups. Groupings: control group, diabetic group, low dose, middle and high dose of mangiferin (15 mg/kg·d, 30 mg/kg·d, 60 mg/kg·d) group. Renal weight, index number of kidney hypertrophy, fasting blood glucose, 24-hour urinary protein excretion and superoxide dismutase (SOD) were observed at 12 week. The structure of kidney were examined by light microscope of hematoxylin-eosin staining (HE). Immunohistochemistry and Western Blot were adopted to detect the expression of transforming growing factor-β(TGF-β), matrix metallo proteinases-2 (MMP-2), tissue inhibitors of matrix metalloproteinase-2 (TIMP-2) in renal tissues.Results①The results of the index number of kidney hypertrophy show that diabetes nephropathy was induced by STZ in rats, the diabetic group compared with normal rats, renal weight and index number of kidney hypertrophy increased significantly (P<0.01), which of mangiferin groups were decreased significantly (P<0.01).②Fasting blood glucose, 24-h urinary protein and SOD showed that the diabetic group compared with normal rats, fasting blood glucose and 24-h urinary protein were significantly increased (P<0.01), SOD activity was significantly down (P<0.01). Fasting blood glucose and 24-h urinary protein of mangiferin groups were significantly decreased (P<0.01), SOD activity was increased (P<0.05 or P<0.01).③The structure of kidney was examined by light microscope of hematoxylin-eosin staining (HE). Compared with control group, mesangial matrix and basement membrane of glomerular proliferated, the number of glomerular cells was increased. Glomerular cavity increases, some parts of glomerular shrinked and fibroticedticed. The cells of tubular expanded and swelled. Treatment of mangiferin can suppress different degrees of disease.④Immunohistochemistry and Western Blot show that diabetes compared with normal, TGF-βand TIMP-2 expression was increased (P<0.01), while MMP-2 expression was significantly decreased (P<0.01). Compared with the diabetic group, mangiferin treatment group TGF-βand TIMP-2 expression were reduced in kidney (P<0.05 or P<0.01), while MMP-2 expression was significantly increased (P<0.01).Conclusions①Mangiferin can relieve the damage of STZ induced diabetic nephropathy (DN) in rats.②The DN protective mechanism of mangiferin may reduce blood glucose and enhance the kidneys antioxidative capability by alleviating oxygen free radical.③Mangiferin may adjust expression of TGF-β, MMP-2, TIMP-2, which are related to regulate metabolism of renal basement membrane and extracellular matrix (ECM) .
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