Department of Physiology, College of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, Anhui Province, China.
Institute of Acu-Moxibustion and Meridian, College of Acupuncture and Tuina, Anhui University of Chinese Medicine, Hefei 230012, Anhui Province, China.
J Integr Med. 2018 Nov;16(6):418-426. doi: 10.1016/j.joim.2018.10.003. Epub 2018 Oct 6.
Acupuncture has a definite therapeutic effect on chronic obstructive pulmonary disease (COPD), and the cholinergic anti-inflammatory pathway (CAP) has been shown to be involved in regulation of inflammation. In this study, we investigated whether electro-acupuncture (EA) affects the CAP in COPD.
Sprague-Dawley rats were induced into COPD through exposure to cigarette smoke combined with lipopolysaccharide. EA treatment was applied at Zusanli (ST36) and Feishu (BL13) points for 30 min/d for 7 d. Seventy-two rats were randomly divided into six study groups, including normal, normal + EA, normal + α-bungarotoxin (α-BGT) (the antagonist of the nicotinic acetylcholine receptor α7 subunit (α7nAChR)) + EA, COPD, COPD + EA, and COPD + α-BGT + EA. Lung function, pathology and vagus nerve discharge were tested. The levels of acetylcholine (ACh), acetylcholinesterase (AChE), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF) and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA and protein expression and immunoreactivity of α7nAChR and its postreceptor inflammation signal pathway, including janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), nuclear factor-κB (NF-κB), were observed by quantitative reverse transcription-polymerase chain reaction, Western blot and immunohistochemistry.
Compared with normal rats, there were a significant decline in lung function and discharge of the vagus nerve (P < 0.01), a marked sign of lung inflammation and an increase of ACh, AChE, IL-6 and TNF-α level in BALF or lung tissue (P < 0.05, P < 0.01) and higher expression of α7nAChR, JAK2, STAT3 and NF-κB (P < 0.05, P < 0.01) in the COPD rats. In rats receiving EA, the lung function and vagal discharge were enhanced (P < 0.01), lung inflammation was improved and the levels of ACh, AChE, IL-6 and TNF-α were decreased (P < 0.01). Further, the expression of α7nAChR, JAK2, STAT3 and NF-κB was downregulated (P < 0.05, P < 0.01). However, the above effects of EA were blocked in rats injected with α-BGT (P < 0.01).
EA treatment can reduce the lung inflammatory response and improve lung function in COPD, which may be related to its involvement in the regulation of CAP.
针刺对慢性阻塞性肺疾病（COPD）有明确的治疗作用，胆碱能抗炎途径（CAP）已被证明参与了炎症的调节。本研究旨在探讨电针对 COPD 中 CAP 的影响。
将 Sprague-Dawley 大鼠暴露于香烟烟雾和脂多糖中，诱导 COPD。EA 治疗应用于足三里（ST36）和肺俞（BL13）点，每天 30 分钟，共 7 天。72 只大鼠随机分为六组，包括正常组、正常+EA 组、正常+α-银环蛇毒素（α-BGT）（烟碱型乙酰胆碱受体α7 亚基（α7nAChR）的拮抗剂）+EA 组、COPD 组、COPD+EA 组和 COPD+α-BGT+EA 组。检测肺功能、病理和迷走神经放电。酶联免疫吸附试验测定支气管肺泡灌洗液（BALF）和肺组织中乙酰胆碱（ACh）、乙酰胆碱酯酶（AChE）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的水平。通过定量逆转录-聚合酶链反应、Western blot 和免疫组织化学观察α7nAChR 及其受体后炎症信号通路，包括 Janus 激酶 2（JAK2）、信号转导和转录激活因子 3（STAT3）、核因子-κB（NF-κB）的 mRNA 和蛋白表达及免疫反应性。
与正常大鼠相比，COPD 大鼠肺功能和迷走神经放电明显下降（P<0.01），肺炎症明显，BALF 或肺组织中 ACh、AChE、IL-6 和 TNF-α水平升高（P<0.05，P<0.01），α7nAChR、JAK2、STAT3 和 NF-κB 的表达增加（P<0.05，P<0.01）。在接受 EA 治疗的大鼠中，肺功能和迷走神经放电增强（P<0.01），肺炎症改善，ACh、AChE、IL-6 和 TNF-α水平降低（P<0.01）。此外，α7nAChR、JAK2、STAT3 和 NF-κB 的表达下调（P<0.05，P<0.01）。然而，在注射α-BGT 的大鼠中，EA 的上述作用被阻断（P<0.01）。
EA 治疗可减轻 COPD 大鼠的肺炎症反应，改善肺功能，这可能与其参与 CAP 的调节有关。
