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[电针干预通过促进慢性阻塞性肺疾病大鼠的免疫调节改善肺功能]

[Electroacupuncture Intervention Improved Pulmonary Function via Promoting Immunoregulation in Chronic Obstructive Pulmonary Disease Rats].

作者信息

Tong Juan, Chen Fu-Chu, Li Gui-Yuan, Kong Xiang-Ao, He Ying, Yao Hong

机构信息

Department of Traditional Chinese Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.

Department of Rehabilitation, the Second Hospital of Nanhai, Foshan City, Foshan 528251, Guangdong Province.

出版信息

Zhen Ci Yan Jiu. 2018 Apr 25;43(4):236-41. doi: 10.13702/j.1000-0607.170424.

DOI:10.13702/j.1000-0607.170424
PMID:29888577
Abstract

OBJECTIVE

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.

METHODS

Forty male SD rats were randomly divided into 5 groups: normal, model, EA, exercise, and EA+ exercise (=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.

RESULTS

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(<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 (<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 (<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 (>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 (< 0.01), and significantly lower in the EA, exercise and EA+exercise groups than in the model group (<0.05), except monocytes in the exercise group (>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 (>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 (<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.

CONCLUSION

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.

摘要

目的

观察电针干预对慢性阻塞性肺疾病(COPD)肌肉萎缩大鼠的免疫调节作用,探讨其改善呼吸功能的潜在机制。

方法

将40只雄性SD大鼠随机分为5组:正常组、模型组、电针组、运动组和电针+运动组(每组8只)。通过将大鼠置于密闭箱中暴露于香烟烟雾(3 - 10支/次)60分钟,每天2次,每周6天,共90天,建立COPD肌肉萎缩模型。从暴露于香烟烟雾后的第80天开始给予电针、运动和电针+运动干预。电针(2Hz/40Hz,6mA)针刺“膻中”(CV17)、“气海”(CV6)、“中脘”(CV12)、“梁门”(ST21)及双侧“曲池”(LI11),每次10分钟,隔日1次,共20次。强迫大鼠在水箱中游泳10分钟进行游泳运动,隔日1次共20次。在麻醉下检测大鼠肺功能,包括吸气阻力(RI)、功能残气量(FRC)、肺动态顺应性(Cdyn)等。采用苏木精-伊红(H.E.)染色检测肺组织病理变化,采用酶联免疫吸附测定(ELISA)法检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)含量。

结果

暴露于香烟烟雾80天后,模型组、电针组、运动组和电针+运动组大鼠体重值均显著低于正常组(P<0.05)。此外,与正常组相比,模型组的RI和FRC水平显著升高,Cdyn水平显著降低(P<0.01)。干预后,与模型组相比,电针组、运动组和电针+运动组的RI和FRC水平均显著下调(P<0.05),提示肺功能有所改善。但3个治疗组的Cdyn降低水平与模型组相比无明显改善(P>0.05)。模型组肺组织单核细胞和淋巴细胞数量以及血清TNF-α、IL-6和IL-1β含量均显著高于正常组(P<0.01),电针组、运动组和电针+运动组均显著低于模型组(P<0.05),运动组单核细胞除外(P>0.05)。电针组、运动组和电针+运动组在RI和FRC水平、肺单核细胞以及血清IL-6和IL-1β方面无显著差异(P>0.05)。运动组和电针+运动组体重显著高于电针组,电针组肺淋巴细胞和血清TNF-α明显低于运动组(P<0.05)。H.E.染色显示建模后支气管管腔变形,支气管黏膜上皮纤毛脱落、扁平,杯状细胞增生,黏膜下层和肌层有大量炎性细胞浸润,支气管血管腔内分泌物增多,肺泡结构不完整,肺泡壁变薄、破裂,肺泡腔扩大形成大的肺大泡,3个治疗组上述改变明显减轻。

结论

电针干预可改善COPD肌肉萎缩大鼠的肺功能和肺组织病理变化,这与其降低肺单核细胞和淋巴细胞数量以及血清TNF-α、IL-6和IL-1β含量有关,提示其增强了免疫调节作用。

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引用本文的文献

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Medicine (Baltimore). 2019 Sep;98(37):e17112. doi: 10.1097/MD.0000000000017112.