The Experimental Research Of The Interference Effect Of Schisandra Chinensis Mixture On Glomerular Fibrosis Progress Of Diabetic Nephropathy Mice

Objective: To investigate the interference effect of Schisandra chinensis mixture(SM) on diabetic nephropathy mice of glomerular fibrosis and to explore its possible mechanisms.Methods:Twenty-four Male,6-7weeks and weights of 20-25g C57BL/6 mice were randomly distributed to 3 groups:normal control group, diabetic nephropathy model group and SM-treated group. Injected STZ into abdomen of mice to establish diabetic mice model. Then the SM-treated group was given SW and other two groups were given water by gavages. Blood glucose, body weight were measured every three weeks. Urinary albumin and urinary creatinine were measured before the mice were killed. Kidney weight were measured when the mice were killed. The morphological changes of renal tissues were observed under microscope. The urinary albumin to urinary creatinine ratio, the kidney to body weight ratio and the glomerulosclerotic injury were calculated. Fibronectin (FN) expressions in kidney tissues were determined by Immunohis- tochemical method. The protein expression of a-smooth muscle actin(a-SMA) in kidney tissues were determined by western blot and the protein expression of a-SMA and cluster of differentiation 31(CD31)in kidney tissues were determined by immunofluorescence labeling.Results:Compared with the corresponding normal control groups, blood glucose were significantly increased, weight decreased, KBWR significantly increased, and ACR and GSI increasing with the progression of diabetes in DM group. In nice week DM model group we could see:glomerular capillary area increased, mesangial expansion, mesangial matrix proliferation and glomerular basement membrane thickening with PASM stain; mesangial area and glomerular area shows a large number of mesangial deposition of extracellular matrix with Masson stain and FN immunohistochemistry; Western blot results showed that:As the disease progre-sses,a-SMA expression continued to increase. CD31 expression continued to decline. Compared with the diabetic model group, SW could significantly reduce ACR, KBWR, GSI(P<0.01 or P<0.05); increaseCD31, reduce a-SMA, expression (P＜0.01); inhibit FN andα-SMA expression in glomerular area; reduce extracellular matrix accumulate in glomerular.Conclusions:SW can inhibit mesangial cell proliferation and myofibroblasts activation. It also can restrain endothelial-to-mesenchymal transition (EndMT), and degrade the accumulation of ECM, and ameliorate glomerular fibrosis.