Abstract
To observe the immunoregulatory effect of electroacupuncture (EA) intervention for muscular dystrophy chronic obstructive pulmonary disease (COPD) rats, so as to investigate its underlying mechanism in improving respiratory function. Forty male SD rats were randomly divided into 5 groups: normal, model, EA, exercise, and EA+ exercise (n=8 in each). The muscular dystrophy COPD model was established by placing the rats in a closed box to be exposed to cigarette smoke (3-10 cigarettes/time) for 60 min, twice daily, 6 days a week for 90 days. The EA, exercise and EA+exercise interventions were given beginning from day 80 after exposure to cigarette smoke. EA (2 Hz/40 Hz, 6 mA) was applied to "Danzhong" (CV 17), "Qihai" (CV 6), "Zhongwan" (CV 12), "Liangmen" (ST 21) and bilateral "Quchi" (LI 11) for 10 min, once every other day, for 20 times. The swimming exercise was conducted by forcing the rat to swim in a water box for 10 min, once every other day, for 20 times. The rat's lung function including the resistance of inspiration (RI), functional residual capacity(FRC), pulmonary dynamic compliance (Cdyn), etc., was detected under anesthesia. Pathological changes of the lung tissue were detected by H.E. staining, and the contents of serum TNF-alpha, IL-6 and IL-1 beta assayed by ELISA. After 80 days' exposure to the cigarette smoke, the rats' body weight values in the model, EA, exercise and EA+exercise groups were significantly lower than that of the normal group(P<0.05). Moreover, the RI and FRC levels were significantly increased, and the Cdyn level was remarkably decreased in the model group relevant to the normal group (P<0.01). Following the intervention, both RI and FRC levels were significantly down-regulated in the EA, exercise and EA+exercise groups relevant to the model group (P<0.05), suggesting an improvement of the lung function. But the decreased Cdyn level had no marked improvement in the 3 treatment groups relevant to the model group (P>0.05). The numbers of monocytes and lymphocytes of the lung tissue, and the contents of serum TNF-α, IL-6 and IL-1 β were significantly higher in the model group than in the normal group (P< 0.01), and significantly lower in the EA, exercise and EA+exercise groups than in the model group (P<0.05), except monocytes in the exercise group (P>0.05). No significant differences were found among the EA, exercise and EA+exercise groups in the levels of RI and FRC, pulmonary monocytes and serum IL-6 and IL-1 β (P>0.05). The body weight was significantly higher in the exercise and EA+exercise groups than in the EA group, and the pulmonary lymphocytes and serum TNF-α obviously lowered in the EA group than in the exercise group (P<0.05). H.E. staining showed deformation of the bronchial tube cavity, detachment and flattening of the bronchial mucosal epithelial cilia, hyperplasia of Goblet cells, infiltration of abundant inflammatory cells in the submucosal layer and muscular layer, more secretions in the bronchovascular cavity, incomplete alveolar structure, thinning and rupture of the alveolar wall, and expansion of the alveolar cavity to form large pulmonary vesicles after modeling, which was obviously milder in the 3 treatment groups. EA intervention can improve the pulmonary function and pathological changes in pulmonary muscular dystrophy COPD rats, which is associated with its effects in reducing pulmonary monocytes and lymphocytes and serum TNF-α, IL-6 and IL-1 β contents, suggesting an enhancement of immunoregulation.
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