Objective: To study preventive effect of Lifei Huaxian Fang

a prescription based on Shengjiang San

on pulmonary fibrosis. And to investigate its effect on signal transduction molecules

transformation of transforming growth factor β1 (factor-β1

have TGF-β1) mediated by Sekclsky mothers against mediated dpp3 (Smad3)

and to clarify the preliminary mechanism responsible for action. Method: One hundred Wistar rats weighing (200±20) g (half male and half female) were divided into 5 groups (n=20 each) randomly. The rats in model group and the treatment group were injected by bleomycin A5 within the trachea to establish pulmonary fibrosis model. Lifei Huaxian Fang administration dosage in the treatment group was 4.41 g ·kg-1 ·d-1. Prednisone administration dosage in the prednisone control group was 1.05 mg ·kg-1 ·d-1. The rats in the prednisone combined with Lifei Huaxian Fang group were ig treated by the above dosages jointly. For normal control group and model group were ig given the same volume of normal saline. By the 7th day and the first 28th day SABC method was applied to detect lung tissue TGF-β1

Smad3 expression in the rats with the help of BI-2000 medical image analysis system. The general situation

body weight and changes in pulmonary coefficient were observed for the rats. Alveolar inflammation and fibrosis degree in lung were evaluated by pathological slides with staining of hematoxylin-Masson. Result: The results suggest the success of mould establishment. The lung inflammation

fibrosis and lungs coefficient were significantly reduced in the treatment group compared with that in the model group. In each of the treated groups

the alveolar degree was lightening obviously

TGF-β1

Smad3 expression were reduced

compared with those in the model group. The effects in the group of combined prednisone with Lifei Huaxian Fang were more obvious. Conclusion: Lifei Huaxian Fang has certain treatment effect for pulmonary fibrosis in the model rats induced by bleomycin A5. The mechanisms may be related to inhibition of the excessive expression of TGF-β1

Smad3.