Department of Physiology and Pathophysiology, Shanghai Medical College of Fudan University, Shanghai, China.
J Integr Med. 2013 May;11(3):213-9. doi: 10.3736/jintegrmed2013024.
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.
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).
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).
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.
有报道称针刺治疗慢性阻塞性肺疾病（COPD）可改善肺功能，但对于其潜在机制知之甚少。由于 COPD 患者可能存在免疫反应失衡，我们假设电针对（EA）可能在调节炎症细胞因子方面发挥作用，并有助于烟雾诱导的 COPD 大鼠模型中的肺保护。
建立雄性 Sprague-Dawley 大鼠吸烟诱导的 COPD 模型。将大鼠随机分为四组（对照组、假手术组、COPD 组和 COPD+EA 组），通过测量肺病理变化和肺功能来评估 COPD 模型。假手术组和 COPD 组大鼠接受足三里（ST36）穴位 EA 治疗，每天 30 分钟，共 14 天。用支气管肺泡灌洗液（BALF）测量肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和丙二醛（MDA）水平。
与对照组大鼠相比，COPD 大鼠的肺阻力（RL）和肺顺应性（CL）明显改变（均 P<0.01），支气管和细支气管气道阻塞（P<0.01），MDA、TNF-α 和 IL-1β 水平也明显升高（均 P<0.01）。对照组和假手术组之间无显著差异。与 COPD 大鼠相比，COPD+EA 大鼠 RL 降低，CL 增加（均 P<0.05），支气管和细支气管气道阻塞减轻（分别为 P<0.05 和 P<0.01），BALF 中 TNF-α、IL-1β 和 MDA 水平降低（均 P<0.05 和 P<0.01）。然而，EA 组大鼠的 TNF-α 和 IL-1β 水平仍高于对照组（P<0.05）。
ST36 处的 EA 可减轻 COPD 大鼠模型中的肺损伤，其有益作用可能与下调炎症细胞因子有关。抗炎和抗氧化作用可能延长 EA 的临床获益。
