Objective To observe the effect of acupoint application on transforming growth factor(TGF)-β1/Smad 3signaling pathway

so as to reveal its mechanism underlying improvement of airway remodeling in chronic asthma mice.Methods BALB/c mice were randomly divided into normal group

model group

sham acupoint application group(sham group)

acupoint application group

and dexamethasone group(n=8in each group).The chronic asthma model was established by intraperitoneal injection of ovalbumin sensitization.The acupoint application group was treated with plaster composed with White Mustard Seed

Rhizoma Corydalis

Unprocessed Radix Kansui

and Herba Asari

on bilateral"Feishu"(BL 13)

"Xinshu"(BL 15)and"Geshu"(BL 17)points

6hours a day for 14 days.The sham group was treated with plaster containing vaseline on bilateral BL 13

BL 15 and BL 17

6hours a day for 14 days.The dexamethasone group was treated with dexamethasone 1mg·kg-1·day-1 intraperitoneally

once daily for 14 days.At the end of treatment

airway resistance was detected by mouse lung function instrument.Patho-logical changes of airway were observed under light microscope after hematoxylin-eosin staining

and the morphological parameters were measured by image analysis software.Immunohistochemistry method was used to detect the expression of TGF-β1and Smad 3in the lung tissue of mice.Results Compared with the normal group

the airway resistance

the total bronchial wall area(WAt)/lumen perimeter(Pi)

the smooth muscle wall area(WAm)/Pi

and the expression of TGF-β1and Smad 3in the lung tissues were significantly higher in the model and sham groups(P<0.01).Compared with the model group and the sham group

the airway resistance

WAt/Pi

WAm/Pi

the expression of TGF-β1and Smad 3in the lung tissues were decreased in the acupoint application group and the dexamethasone group(P<0.05).There were no significant differences between the acupoint application group and the dexamethasone group in the above mentioned indexes(P>0.05).Conclusion Acupoint application can improve airway remodeling by down-regulating the expression of TGF-β1/Smad 3in the airway of chronic asthmatic mice.