Objective    To explore the mechanism of Shenkangwan in preventing the development of diabetic nephropathy (DN) through TGF-β1/Smad signaling pathway.     Methods    The diabetic rat models were established by intraperitoneal injection of streptozotocin (STZ) in male Wistar rats and randomly divided into 3 groups: model control group

Capoten group and Shenkangwan group. Another 8 normal Wistar rats served as normal control. After the rats had been treated for 8 weeks

the mRNA expressions of fibronetin (FN) and TGF-β1 were detected by RT-PCR and the protein expressions of Smad 2

Smad 3 by immunohistochemistry in the renal tissues.     Results    During the past 8 weeks

the blood glucose of the rats in the model control group was all over 16.7 mmol/L and they exhibited the symptoms of diabetes mellitus

such as excessive thirsty

extreme hunger

frequent urination and unusual weight loss. The mRNA expressions of FN and TGF-β1 in rat renal tissues of model control group were significantly higher than those in the rats of normal control group (P0.01)

accompanied by the increased quantity of the cells positive of Smad 2 and Smad 3 in their kidneys. Compared with model control group

the mRNA expressions of FN and TGF-β1 as well as the protein expressions of Smad 2 and Smad 3 in the rat kidney tissues of Shenkangwan and capoten groups were significantly decreased (P0.01).     Conclusion    Shenkangwan can restrain the activation of TGF-β1/Smad signaling pathway and reduce the synthesis and secretion of extracellular matrix in the renal tissues of DN rats

which would conduce to postphone the development of DN.