title: Effects of electroacupuncture at Zusanli (ST36) on inflammatory cytokines in a rat model of smoke-induced chronic obstructive pulmonary disease.
abstract: OBJECTIVE
  Improvement in lung function was reported after acupuncture treatment of chronic obstructive pulmonary disease (COPD), but little is known about the underlying mechanisms. Because an immune response imbalance could be seen in COPD, we hypothesize that electroacupuncture (EA) may play a role in regulating inflammatory cytokines and contribute to lung protection in a rat model of smoke-induced COPD.
  
  
  METHODS
  A COPD model using male Sprague-Dawley rats exposed to cigarette smoke was established. The rats were randomly divided into four groups (control, sham, COPD, and COPD plus EA), and COPD model was evaluated by measuring pulmonary pathological changes and lung function. EA was applied to the acupuncture point Zusanli (ST36) for 30 min/d for 14 d in sham and COPD rats. Bronchoalveolar lavage fluid (BALF) was used to measure levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and malonaldehyde (MDA).
  
  
  RESULTS
  Compared with the control rats, COPD rats had significant changes in lung resistance (RL) and lung compliance (CL) (both P<0.01), bronchi and bronchiole airway obstruction (P<0.01), and levels of MDA, TNF-α, and IL-1β (P<0.01). There were no significant differences between the control and the sham groups. Compared with the COPD rats, the COPD plus EA rats had decreased RL and increased CL (both P<0.05), and reduced bronchi and bronchiole airway obstruction (P<0.05, P<0.01, respectively), while levels of TNF-α, IL-1β, and MDA in BALF were lowered (P<0.05 and P<0.01, respectively). However, TNF-α and IL-1β levels of the EA group rats remained higher than those of the control group (P<0.05).
  
  
  CONCLUSIONS
  EA at ST36 can reduce lung injury in a COPD rat model, and beneficial effects may be related to down-regulation of inflammatory cytokines. The anti-inflammatory and antioxidant effects may prolong the clinical benefit of EA.
authors.affiliation: Department of Physiology and Pathophysiology, Shanghai Medical College of Fudan University, Shanghai, China.
authors.forename: Wen-ye
authors.initials: WY
authors.lastname: Geng
authors.forename: Zi-bing
authors.initials: ZB
authors.lastname: Liu
authors.forename: Na-na
authors.initials: NN
authors.lastname: Song
authors.forename: Wen-ye
authors.initials: WY
authors.lastname: Geng
authors.forename: Gui-hong
authors.initials: GH
authors.lastname: Zhang
authors.forename: Wei-zhong
authors.initials: WZ
authors.lastname: Jin
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Yin-Xiang
authors.initials: YX
authors.lastname: Cao
authors.forename: Da-Nian
authors.initials: DN
authors.lastname: Zhu
authors.forename: Lin-Lin
authors.initials: LL
authors.lastname: Shen
mesh_terms: D015669:Acupuncture Points; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D004195:Disease Models, Animal; D015671:Electroacupuncture; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology*; D008297:Male; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000276:immunology* / Q000628:therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012907:Smoking / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha