Objective: To study the effect of modified Erchentang on expression of Smad3

4

6

7 genes in the lung tissue of rats with chronic obstructive pulmonary disease (COPD). Method: Fifty SD rats were randomly divided into normal group

model group

and low

middle and high-dose modified Erchentang groups (5

10

20 g·kg-1·d-1). COPD model in rats was prepared by using cigarette smoke and dripping lipopolysaccharide (LPS) in trachea. After the modeling

normal and model groups were given normal saline solution through intragastric administration

while other groups were given corresponding herbal drugs intragastrically (5

10.20 g·kg-1·d-1) for 14 days. The pulmonary function was evaluated [forced vital capacity (FVC)

at the end of the first seconds forced expiratory volume (FEV1)]. The expressions of Smad3

Smad4

Smad6 and Smad7 mRNA were detected by quantitative real time PCR (Real-time PCR) method

and immunohistochemistry (IHC) method was used to detect the expression of Smad3

Smad4

Smad6

Smad7

TGF-β1 and it's receptor (TGF-beta RI) protein in the lung tissue of all of the groups. Result: Compared with normal group

FVC

FEV1 and FEV1/FVC of the model group were decreased significantly (P<0.01); the expression of Smad3 and Smad4 mRNA and was increased (P<0.05)

the expression of Smad4 and Smad3 protein was incr eased significantly (P<0.01)

the expression of Smad6 and Smad7 mRNA was decreased (P<0.05)

the expression of Smad7 and Smad6 protein was decreased significantly (P<0.01) in model group. Compared with model group

FVC

FEV1 and FEV1/FVC index were increased significantly (P<0.01)

the expression of Smad3 and Smad4 mRNA was decreased (P<0.05)

the expression of Smad3 and Smad4 protein was decreased significantly (P<0.01)

but the expression of Smad6 and Smad7 mRNA was increased (P<0.05)

Smad6 and Smad7 protein was increased significantly (P<0.01)

in modified Erchentang of 10 g·kg-1·d-1 and 20 g·kg-1·d-1groups. Conclusion: Modified Erchentang can effectively inhibit bronchial remodeling

and improve pulmonary ventilation of COPD. Its mechanism may be correlated with reduction of Smad3 gene expression

increase of the expression of Smad6 and Smad7 genes

coordination of Smad4 gene expression and inhibition of the expression of bronchioles and pulmonary tissue remodeling.