OBJECTIVE： 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 imba...OBJECTIVE： 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. METHODS： 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-a （TNF-a）, interleukin-113 （IL-113）, and malonaldehyde （MDA）. RESULTS： Compared with the control rats, COPD rats had significant changes in lung resistance （R,） and lung compliance （C,） （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 R, 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）. CONCLUSION： 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.展开更多
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 regula- tion of infla...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 regula- tion 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 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-ct） in bronchoalveolar lavage fluid （BALF） and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA and protein expression and immunoreac- tivity of α7nAChR and its postreceptor inflammation signal pathway, including janus kinase 2 （JAK2）, sig- nal transducers and activators of transcription 3 （STAT3）, nuclear factor-KB （NF-KB）, 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-α level in BALF or lung tissue （P 〈 0.05, P 〈 0.01 ） and higher expression of 0t7nAChR, JAK2, STAT3 and NF-αB （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-BCT （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.展开更多
Inflammation and lung function decline are the main pathophysiological features of chronic obstructive pulmonary disease （COPD）. Acupuncture can improve lung function in patients with COPD, but the underlying mechan...Inflammation and lung function decline are the main pathophysiological features of chronic obstructive pulmonary disease （COPD）. Acupuncture can improve lung function in patients with COPD, but the underlying mechanisms are not well understood. Orexins （OXs）, which are found in peripheral plasma, are neuropeptides that regulate respiration and their levels are related to COPD. Therefore, we hypothesized that acupuncture might alter OXs, reduce lung inflammation and improve lung function in COPD. METHODS： COPD was induced in rats by exposure to cigarette smoke for 8 weeks and injecting with lipopolysaccharide twice. Electroacupuncture （EA） was performed at Feishu （BL13） and Zusanli （ST36） for 30 min/d for 2 weeks. Rat lung function and morphology were assessed after EA. The levels of tumor necrosis factor-α （TNF-a） and intedeukin-1β （IL-16） in bronchoalveolar lavage fluid （BALF） and orexin A and B levels in the lung tissue were detected by enzyme-linked immunosorbent assay. OX receptor mRNA levels and immunopositive cells were assessed with real-time polymerase chain reaction and immunohistochemical methods, respectively. The relationships among lung function, cell factors, and OX levels were analyzed by Pearson correlation analyses. RESULTS： Compared with the control group, lung function was significantly decreased in the rats with COPD （P〈0.05）. There were obvious increases in TNF-α and IL-1β levels in BALF （P〈0.05 and P〈0.01, respectively）, orexin A level in lung tissue （P〈0.01; but not orexin B） and mRNA expressions of OX 1 type receptor （OXR1） and OX 2 type receptor （OXR2） in lung tissue （P〈0.05 and P〈0.01, respectively）; the integrative optical densities （IODs） of both receptors were greater in the COPD group （P〈0.05）. For rats with COPD subjected to EA, lung function was improved （P〈0.05）. There were notable decreases in TNF-a and IL-1β levels （P〈0.05 and 〈0.01, respectively） in BALF. Orexin A, but not orexin B, levels in lung tissue also decreased （P〈0.01）, as did mRNA expression of OXlR and OX2R in lung tissue （P〈0.05 and P〈0.01, respectively）. Receptor IODs were also reduced after EA treatment （P〈0.05）. Furthermore, orexin A levels and ratio of forced expiratory volume in 0.3 s to forced vital capacity were strongly negatively correlated （P〈0.01）, and orexin A was positively correlated with TNF-α and IL-1β （P〈0.001 and P〈0.05, respectively）.CONCLUSION： EA at Zusanli and Feishu improved lung function of rats with COPD and had an anti-inflammatory effect, which may be related to down-regulation of OXA and its receptors.展开更多
基金supported by grants from the National Natural Science Foundation of China(No.81070001,No. 30670771)the Science and Technology Commission of Shanghai Municipality(No.09JC1402100,No.07DZ19722- 3)+1 种基金the Shanghai Leading Academic Discipline Project (No.B112)the Shanghai MICCA1 Key Laboratory (No.06DZ22103)
文摘OBJECTIVE： 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. METHODS： 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-a （TNF-a）, interleukin-113 （IL-113）, and malonaldehyde （MDA）. RESULTS： Compared with the control rats, COPD rats had significant changes in lung resistance （R,） and lung compliance （C,） （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 R, 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）. CONCLUSION： 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.
基金supported by grants from the National Natural Science Foundation of China(No. 81373743)Outstanding Young Talents Support Program of Anhui(No. 20140181)
文摘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 regula- tion 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 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-ct） in bronchoalveolar lavage fluid （BALF） and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA and protein expression and immunoreac- tivity of α7nAChR and its postreceptor inflammation signal pathway, including janus kinase 2 （JAK2）, sig- nal transducers and activators of transcription 3 （STAT3）, nuclear factor-KB （NF-KB）, 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-α level in BALF or lung tissue （P 〈 0.05, P 〈 0.01 ） and higher expression of 0t7nAChR, JAK2, STAT3 and NF-αB （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-BCT （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.
基金supported by grants from the National Natural Science Foundation of China(No.81072870No.81102660+1 种基金No.81373743)Open Research Fund of Zhejiang First-foremost Key Subject-Acupuncture&Moxibustion(No.ZTK2010B06)
文摘Inflammation and lung function decline are the main pathophysiological features of chronic obstructive pulmonary disease （COPD）. Acupuncture can improve lung function in patients with COPD, but the underlying mechanisms are not well understood. Orexins （OXs）, which are found in peripheral plasma, are neuropeptides that regulate respiration and their levels are related to COPD. Therefore, we hypothesized that acupuncture might alter OXs, reduce lung inflammation and improve lung function in COPD. METHODS： COPD was induced in rats by exposure to cigarette smoke for 8 weeks and injecting with lipopolysaccharide twice. Electroacupuncture （EA） was performed at Feishu （BL13） and Zusanli （ST36） for 30 min/d for 2 weeks. Rat lung function and morphology were assessed after EA. The levels of tumor necrosis factor-α （TNF-a） and intedeukin-1β （IL-16） in bronchoalveolar lavage fluid （BALF） and orexin A and B levels in the lung tissue were detected by enzyme-linked immunosorbent assay. OX receptor mRNA levels and immunopositive cells were assessed with real-time polymerase chain reaction and immunohistochemical methods, respectively. The relationships among lung function, cell factors, and OX levels were analyzed by Pearson correlation analyses. RESULTS： Compared with the control group, lung function was significantly decreased in the rats with COPD （P〈0.05）. There were obvious increases in TNF-α and IL-1β levels in BALF （P〈0.05 and P〈0.01, respectively）, orexin A level in lung tissue （P〈0.01; but not orexin B） and mRNA expressions of OX 1 type receptor （OXR1） and OX 2 type receptor （OXR2） in lung tissue （P〈0.05 and P〈0.01, respectively）; the integrative optical densities （IODs） of both receptors were greater in the COPD group （P〈0.05）. For rats with COPD subjected to EA, lung function was improved （P〈0.05）. There were notable decreases in TNF-a and IL-1β levels （P〈0.05 and 〈0.01, respectively） in BALF. Orexin A, but not orexin B, levels in lung tissue also decreased （P〈0.01）, as did mRNA expression of OXlR and OX2R in lung tissue （P〈0.05 and P〈0.01, respectively）. Receptor IODs were also reduced after EA treatment （P〈0.05）. Furthermore, orexin A levels and ratio of forced expiratory volume in 0.3 s to forced vital capacity were strongly negatively correlated （P〈0.01）, and orexin A was positively correlated with TNF-α and IL-1β （P〈0.001 and P〈0.05, respectively）.CONCLUSION： EA at Zusanli and Feishu improved lung function of rats with COPD and had an anti-inflammatory effect, which may be related to down-regulation of OXA and its receptors.
