Objective To observe the effect of electroacupuncture(EA)at"Zusanli"(ST 36)and"Feishu"(BL 13)on pulmonary function

inflammatory reaction and expression of macrophage migration inhibitory factor(MIF)and its receptor complex CD 74-CD 44

etc.in rats with chronic obstructive pulmonary disease(COPD)

so as to explore its mechanism underlying improvement of COPD.Methods Thirty male SD rats were randomly divided into normal

model and EA groups(n=10 in each group).The COPD model was established by intratracheal infusion of Lipopolysaccharide(LPS

1 mg/mL)and forced smoke-inhaling.EA was applied to bilateral ST 36 and BL 13 for 30 min

once daily for 7 days.The rats lung function(forced vital capacity[FVC]

forced expiratory capacity ratio([FEV 0.1/FVC]and[FEV 0.3/FVC])was detected under anesthesia.Pathological changes of the lung tissue were detected by H.E.staining

and the contents of MIF

tumor necrosis factor-α(TNF-α)

interleukin-1β(IL-1β)and IL-8 in serum

bronchoalveolar lavage fluid(BALF)and lung tissue were assayed by ELISA.The immunoactivity of CD 74 and CD 44 was detected by immunohistochemistry

and the expression levels of MIF

CD 74

CD 44 and p 38 MAPK mRNAs and proteins were examined by quantitative RT-PCR and Western blot

respectively.Results Compared with the normal group

the FVC

FEV 0.1

FEV 0.3

FEV 0.1/FVC and FEV 0.3/FVC levels were significantly decreased in the model group(P<0.01).After EA treatment

the FVC

FEV 0.1

FEV 0.3

FEV 0.1/FVC and FEV 0.3/FVC were significantly increased(P<0.01

P<0.05)

suggesting an improvement of the pulmonary function after EA.H.E.staining showed that the severity of modeling induced alveolar expansion and inflammatory cell infiltration in the lung tissue was relatively milder in the EA group relevant to the model group.The contents of MIF

TNF-α

IL-1βand IL-8 in the serum

BALF and lung tissues were significantly higher in the model group than in the normal group(P<0.01)

and significantly down-regulated in the EA group relevant to the model group(P<0.01).The expression levels of MIF

CD 74

CD 44 and p 38 MAPK mRNAs and proteins and the immunoactivity levels of CD 74

CD 44 in the lung tissue were obviously higher in the model group than those in the normal group(P<0.01)

and considerably lower in the EA group than those in the model group(P<0.01).There was a positive correlation between p 38 MAPK and MIF in mRNA and protein expression levels(P<0.01).Conclusion EA intervention can improve the pulmonary function in COPD rats

which may be related to its effects in inhibiting inflammatory reaction

and MIF/CD 74-CD 44/p 38 MAPK signaling pathway.