The Correlative Factors Of Tubulointerstitial Lesions And The Function Mechanism Of Shen Shu Ning Of Smoothing Shao Yang In Mesangial Proliferative Glomerulonephritis Rats

BACKGROUND: Tubulointerstitial lesions is the leading cause of end-stage renal failure(ESRF). Its happening and developing is from the result of various factor interactions such as the infiltration of inflammation,the production of cell factor, the phenotype transdifferentiation of renal cell and the deposition of extracelluar matrix etc. In this study, we used a new animal model of progressive tubulointerstitial injury(TII) induced by injecting steophylococcus enterotoxin into rat caudal vein, feeding bovine serum albumin every other day, subcutaneous injection Freunds adjuvant periodically to make the modelof Mesangial proliferative glomerulonephritis(MsPGN) rats and develop to tubulointerstitial lesion model. Using this new model of progressive TII, we observed the law of change of tubulointerstitial lesions and interactions between each factor, examined the hypothesis that Shen Shu Ning(SSN) of Smoothing Shao Yang(SSY) prevented the progression to TII by modulating the effects on the production of transforming growth factor-betal (TGF-β₁) and connective tissue growth factor(CTGF) and platelet derived growth factor (PDGF) and monocyte/macrophage(CD68⁺) and proliferating cell nuclear antigen(PCNA) and α-smooth muscle actin(α-SMA) and plasminogen activator inhibitor-1 (PAI-1)and extracellular matrix components(C01II, FN). METHODS: We studied the effect of SSN of SSY on the clinical features and morphological lesions in the rat model, at the same time, used benazeprii as control. After 12 weeks and 16 weeks of treatment witn SSN and an benazeprii, we examined 24 hours proteinuria and urine microalbumin and urine β -D-N-Acetyl glucosaminidase(NAG) and urine β-D-galactosidase (GAL) and urine β₂-microglobulin(β₂-MG) and blood urine nitrogen (BUN) and serum creatinine(Scr) and the renal morphology and ultrastructure and the...