Objective: To investigate the effect of Heshen pill (HSP) on urinary protein and the expression of nephrin protein in rats with adriamycin-induced nephropathy. Method: The rats were randomly divided into four groups

namely the model group

the HSP group (1.8 g·kg-1)

the benazepril group (1 mg·kg-1) and the control group. Nephropathy rat model was induced through injection of adriamycin (6 mg·kg-1). After successful modeling

the HSP group and the benazepril group were giventhe corresponding drugs

and the model group and the control group were given equivalent volume of distilled water

1 times a day

for 28 days. At the end of the experiment

24 h urine was collected for urine protein detection

and aortic blood was collected for albumin(Alb)

serum creatine(SCr)

blood urea nitrogen(BUN) detection. The morphological changes in renal tissues were assessed by hematoxylin-eosin (HE) staining

and the changes in foot process and basilar membrane of podocytes were probed under transmission electron microscope (TEM). The nephrin protein was measured by immunohistochemistry and Western blot. Result: After the treatment

the 24 h proteinuria of the HSP group was decreased significantly than that of the model group (P<0.01). SCr

BUN were decreased significantly

and Alb was increased significantly of the HSP group than those of the model group (P<0.01). Histopathological examination revealed that glomerular epithelial cell swelling of the HSP group was reduced significantly

glomerular volume was increased slightly

mesangial cells and matrix showed slight hyperplasia

and no protein cast is found in lumen. Ultrastructural examination showed that the glomerular basement membrane of the HSP group was smooth and even

with slight thickening

and foot process was clear and complete

with occasional fusion. Immunohistochemistry showed that the positive area rate of nephrin protein of the HSP group was significantly superior to that of the model group (P<0.01). Western blot demonstrated that the nephrin protein expression of the HSP group was significantly superior to that of the model group (P<0.01). Conclusion: The inhibitive effects of HSP on proteinuria are achieved by promoting nephrin expression and repairing podocyte damage.