Zhang_2018_J.Integr.Med_16_418

OBJECTIVE: 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. METHODS: 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 30min/d for 7d. Seventy-two rats were randomly divided into six study groups, including normal, normal+EA, normal+alpha-bungarotoxin (alpha-BGT) (the antagonist of the nicotinic acetylcholine receptor alpha7 subunit (alpha7nAChR))+EA, COPD, COPD+EA, and COPD+alpha-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-alpha (TNF-alpha) in bronchoalveolar lavage fluid (BALF) and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA and protein expression and immunoreactivity of alpha7nAChR and its postreceptor inflammation signal pathway, including janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), nuclear factor-kappaB (NF-kappaB), were observed by quantitative reverse transcription-polymerase chain reaction, Western blot and immunohistochemistry. RESULTS: 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-alpha level in BALF or lung tissue (P<0.05, P<0.01) and higher expression of alpha7nAChR, JAK2, STAT3 and NF-kappaB (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-alpha were decreased (P<0.01). Further, the expression of alpha7nAChR, JAK2, STAT3 and NF-kappaB was downregulated (P<0.05, P<0.01). However, the above effects of EA were blocked in rats injected with alpha-BGT (P<0.01). CONCLUSION: 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.