Objective: To explore effects of tanshinone ⅡA on expression changes of nephrin and transforming growth factor-β1(TGF-β1)in adriamycin(ADR)-induced-nephropathy rats. Method: Fifty-six rats of Sprague-Dawley were divided into two groups:the model group(n=44)and the control group(n=12).The rats in the model group were injected with a single dose of ADR(0.007 g·kg-1)via tail-vein

while the rats in the control group were injected with a comparable volume of 0.9% saline. The model was successfully established when the 24 h urinary protein excretion exceeded 100 mg after ADR injection 1 week

forty rats were successful and then were randomly assigned to the ADR nephrosis group(n=10)

prednisone group(n=10)

the low dose and high dose of tanshinone ⅡA group(n=10). The rats in the prednisone group were treated with prednisone(0.01 g·kg-1·d-1)

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The rats in the low dose and high dose of tanshinone ⅡA group were treated with tanshinone ⅡA(0.02 g·kg-1·d-1 or 0.04 g·kg-1·d-1)

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once a day for 4 weeks

whereas the other rats were received a comparable volume of 0.9% saline. The blood and urina biochemical indicators were measured and the pathological changes of the renal tissues were observed under light microscope

immunohistochemical and Western blotting techniques to detect the expression of nephrin and TGF-β1. Result: The 24 h urinary protein

cholesterol

triglyceride

blood urea nitrogen

serum creatinine

and the expression of TGF-β1 in the ADR nephrosis group

prednisone group

the low dose and high dose of tanshinone ⅡA group were higher than those in the control group(P<0.05). The total protein

albumin and the expression of nephrin in the ADR nephrosis group

prednisone group

the low dose and high dose of tanshinone ⅡA group was lower than those in the control group(P<0.05). After treatment with prednisone and the high dose of tanshinone ⅡA could improve above-mentioned indicators. Conclusion: Nephrin and TGF-β1 play an important role in the pathogenesis of ADR nephrosis; tanshinone ⅡA decreased the urine albumin excretory rate

and prevent the glomemlar sclerosis in rats with ADR nephrosis

which mechanism may be at least partly correlated with enhancing the expression of nephrin and inhibiting the expression of TGF-β1 in kidney.