Objective To observe the effect of electroacupuncture(EA) at "Zusanli"(ST36) and "Feishu"(BL13) on M1 polarization of alveolar macrophages(AM) in rats with chronic obstructive pulmonary disease(COPD)

so as to explore its anti-inflammatory mechanism underlying improvement of COPD. Methods Forty SD rats were randomly divided into normal and normal+EA

COPD model and COPD+EA groups(n=10 in each group). The COPD model was established by simple fumigation. EA(4 Hz/20 Hz

1 to 2 mA) was applied to bilateral ST36 and BL13 for 30 min

once every other day for 2 weeks. The pulmonary function including the forced vital capacity(FVC)

forced expiratory volume in 0.1 and 0.3 s(FEV0.1

FEV0.3

FEV0.1/FVC

and FEV0.3/FVC) was detected by using a small animal respiratory function detector. Histopathological changes of the lung were displayed by H.E. staining. The contents of tumor necrosis factor-α(TNF-α) and induced nitric oxide synthase(iNOS) in the broncho alveolar lavage fluid(BALF) were assayed by ELISA. The expression of M1 polarization markers(CD86

iNOS)

myeloid differentiation factor 88(MyD88) and nuclear factor-κB p65(NF-κB p65) in AM were detected by Western blot and quantitative real time-PCR

separately. The distribution and expression of CD86 in the lung were detected by immunohistochemistry. Results Following modeling

the levels of FVC

FEV0.1

FEV0.3

ratios of FVE0.1/FVC and FEV0.3/FVC were significantly decreased(P<0.01)

while the contents of TNF-α and iNOS in the BALF

expression of CD86

iNOS

MyD88 and NF-κB p65 mRNAs and proteins in the AM

and CD86 immunoactivity in the lung were significantly increased in the model group relevant to the normal group(P<0.01). After the intervention

the decrease of the lung function and increase of the above-mentioned genes and proteins were all reversed in the COPD+EA group(P<0.05

P<0.01). Conclusion EA at ST36 and BL13 can reduce pulmonary inflammation in COPD rats

which may be related to its function in inhibiting M1 polarization of AM via down-regulating MyD88/NF-κB p65 signaling pathway.