Objective To investigate the protective function of oxymatrine on the renal intestitial fibrosis in rats.Methods Forty male Sprague Dawley rats were randomly divided into 5 groups: sham group,model group,Lotensin group,large-dose oxymatrine group,and small-dose oxymatrine group.The models were established by unilateral ureteral obstruction(UUO) of the left side.On the 14~(th) day after operation,the obstructed kidney was taken out.Then,HE,Massion,and immunohistochemistry staining of transforming growth factor-?_(1)(TGF-?_(1)),(?-smooth) muscle acting(?-SMA) and collagen Ⅲ were conducted.After that,semiquantitative analysis was performed.Results After oxymatrine,treatment,the expressions of ?-SMA,TGF-?_(1) and ColⅢ of the obstructed kidney in the treatment group were significantly lower than those in the model group(P0.05).Conclusion Oxymatrine may reduce the expression of cytokines such as TGF-?_(1),then the activation of cell producing ECM and then the sendimentation of ECM,thus preventing renal interstitial fibrosis.

Objective To study the effect of Benazepril on the renal connective tissue growth factor(CTGF) expression and interstitial fibrosis in unilateral ureteral obstruction(UUO) rats and to illuminate the possible mechanisms.Methods 24 Sprague-Dawley rats were randomly divided into Sham-operated,control and Benazepril groups.From the day before operation,the rats were under intragastric administration of Benazepril 10mg/(kg?d) in Benazepril group,and sodium chloride in tales doses in Sham and control groups.On the 14~(th) day after operation,the obstructed kidney was taken out to be measured by HE,Masson,and immunohistochemistry staining for TGF-?_1,CTGF,?-SMA and ColⅢ.Results The score of renal interstitial lesion and fibrosis index in Benazenpril were significantly lower than those in the control group(P

Objective To investigate the effect of all-trans retinoic acid(atRA) on the urinary TGF?_1 excretion and glomerular lesion of diabetic rats at early stage.Methods SD rats were randomly assigned into 3 groups: atRA treated group,diabetic control group and normal control group.Streptozotocin(STZ)-induced early diabetic male SD rat were used.The atRA treated group were treated with daily subcutaneous injections atRA of 10mg/kg for 7 days(n=6),and then the excretion of urinary protein and TGF?_1 and NO level of plasma,urine and renal tissue were measured,and pathological changes of their kidneys were observed.Results The diabetic control rats showed increased urinary excretion of protein and TGF?_1 and NO level of plasma,urine and renal tissue and deposit of glomerular matrix,while atRA prevented these changes.Conclusion AtRA can prevent the development of diabetic nephropathy,which is relevant with the inhibition of secretion of TGF?_1 and NO.

Objective To investigate the effect of at-RA in macrophage accumulation in tubulointerstitium of rats with renal tubulointerstitial fibrosis.Methods Unilateral ureteral obstructive(UUO) rat animal models were used for the study.40 SD rats were randomly divided into 5 groups: sham group,UUO group,benazepril group,low-dose at-RA groups and high-dose at-RA groups.The rats were under intragastric administration by benazepril(10mg/(kg?d)) in benazepril group,and by(at-RA)(10mg/(kg?d)) in low-dose at-RA group and 20mg/(kg?d) in high-dose at-RA group and by sodium chloride in tales doses in sham group and UUO group from the day before the operation to 14 day after operation.Immunohistochemistry staining of CD68 and Col Ⅲ was used to define the macrophage accumulation and expression of interstitial Col Ⅲ.The degree of tubulointerstitial damage was scored by HE and Masson staining.Results Tubulointerstitial macrophage infiltration were all significantly reduced by(at-RA) or benazepril treatment.They also improved the histological changes of UUO rats and inhibited interstitial colⅢ deposition.Conclusion Reduction of interstitial macrophage infiltration may be an important event by which(at-RA) or benazepril prevents renal injury caused by UUO.