Objective To observe the effect of electroacupuncture(EA) at "Zusanli"(ST36) on the expression of epidermal growth factor receptor(EGFR)

tumor necrosis factor α(TNF-α) transfer growth factor α(TGF-α)

interleukin-8(IL-8)

p38 mitogen-activated protein kinases(p38 MAPK)

mucin-5 AC(MUC5 AC) and other related factors in chronic obstructive pulmonary disease(COPD) rats

so as to reveal its underlying mechanisms in improving COPD. Methods A total of thirty male SD rats were randomly divided into normal control

model and EA groups

with 10 rats in each group. The COPD model was replicated using a combined method of tracheal infusion of lipopolysaccharide(LPS) and forced smoke-inhaling. EA(1—3 mA

4 Hz/20 Hz) was applied to bilateral ST36 for 30 min

once daily for two consecutive weeks. The lung ventilation activities including the forced vital capacity(FVC) and forced expiratory volume(FEV) at 0.1 and 0.3 s(FEV0.1

FEV0.3) were detected. Histopathological changes of the middle lobe and bronchus of the right lung were observed after H.E. staining. The contents of TGF-α

TNF-α and IL-8 in the serum

bronchoalveolar lavage fluid(BALF) and superior lobe of the right lung were assayed by using ELISA

and the expression levels of EGFR

p38 MAPK and MUC5 AC proteins(inferior lobe of the left lung) and mRNAs(inferior lobe of the right lung) detected using Western blot

immunohistochemistry(strept avidin-biotin complex

SABC method) and real-time quantitative PCR

respectively. Results Compared with the normal group

the FVC

FEV0.1

FEV0.3

FEV0.1/FVC and FEV0.3/FVC levels were significantly decreased(P<0.01)

while the contents of TNF-α

TGF-α and IL-8 in the serum

BALF and lung tissues

expression levels of EGFR

p38 MAPK and MUC5 AC mRNAs and proteins

and the immunoactivity of EGFR

p38 MAPK and MUC5 AC in the lung tissues were significantly increased in the model group(P<0.01). After EA intervention

the decreased levels of the FVC

FEV0.1

FEV0.3

FEV0.1/FVC and FEV0.3/FVC

and the increased levels of the abovementioned genes and proteins were all reversed in the EA group(P<0.01

P<0.05). After modeling

the bronchial walls were thickened

with enlarged alveolar cavities

fractured alveolar walls

obvious inflammatory cell infiltration

and rich mucus secretion in the lumen

which was relatively milder in the EA group. Conclusion EA of ST36 can improve the ventilation function in COPD rats

which may be associated with its function in down-regulating the levels of TNF-α

TGF-α

IL-8

EGFR

p38 MAPK and MUC5 AC mRNAs and proteins in the lung tissues

inhibiting EGFR-p38 MAPK signaling mediated expression of MUC5 AC.