Objective: To observe the effect of modified Erchentang on gene expression of transforming growth factor-β1(TGF-β1) and its receptor TGF-βRⅡ in lung tissue

the expression of mRNA and activity of histone deacetylase 2 (HDAC2) in peripheral blood mononuclerar cells (PBMCs) of rats with chronic obstructive pulmonary disease (COPD). Method: The method of smoke combined with lipopolysaccharide (LPS) was used to prepare COPD model in rats. The experimental animals were randomly divided into normal control group

model group

high

middle and low-dose modified Erchentang groups (20

10

5 g·kg-1). Normal group and model group were orally given normal saline (10 g·kg-1)

and high

middle and low-dose modified Erchentang groups were orally given the drug for consecutively 14 days. The activity of HDAC2 was determinate by Enzyme-linked immune fluorescence. Euzyme-linked immunosorbent assay was used to determine the levels of TGF-β1 in lung homogenates and histone deacetylase 2 (HDAC2) in peripheral blood mononuclerarcells (PBMCs) of all groups before and after treatment. Real-time fluorescence quantitative PCR (Real-time PCR) method was used to detect the expression of TGF-β1 mRNA and HDAC2 mRNA. Immunohistochemical (IHC) detection was performed for the expression of TGF-β1 and TGF-βRⅡ protein in lung tissues. Result: Compared with the normal group

the levels of TGF-β1 was significantly increased (P<0.05)

expression of TGF-β1 mRNA

and TGF-β1 and TGF-βRⅡ protein expressions in lung homogenates were significantly higher (P<0.01)

while the expression of mRNA

content and activity of HDAC2 in PBMCs were decreased significantly in model group

with statistically significant differences. Compared with the model group

expressions of TGF-β1 mRNA (P<0.01) and TGF-βRⅡ protein in lung tissue of the rats treated with high and middle-dose modified Erchentang(20

10 g·kg-1) were decreased significantly (P<0.05

P<0.01)

TGF-β1 and TGF-βRⅡ protein expressions were lower than model group (P<0.01)

the expression of HDAC2 mRNA

content and activity of HDAC2 were higher significantly (P<0.05

P<0.01)

with statistical significance and obvious improvement in lung tissue structures. Conclusion: Modified Erchentang has an anti-inflammatory effect on COPD. Its mechanism may be correlated with inhibition of expression of TGF-β1 and TGF-β receptor Ⅱ genes

improvement of the expression and activity of HDAC2 in PBMCs

and inhibition of the inflammatory response.