沙美特罗氟替卡松对抗COPD患者线粒体氧化磷酸化功能障碍的研究
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摘要
目的:探讨沙美特罗氟替卡松对抗COPD患者成肌细胞线粒体氧化磷酸化功能障碍的机制。方法:选取2010年4月至2013年8月医院100例COPD稳定期患者纳入本研究并进行为期1.5年的随访,随访结束后将其中坚持使用沙美特罗氟替卡松的44例设为观察组,余下56例设为对照组,将同期健康体检的50例设为健康组。检测三组肺功能、外周血肿瘤坏死因子((Tumor Necrosis Factorα,TNF-α)浓度变化,单核细胞线粒体氧化磷酸化复合体的表达变化以及三组单核细胞形态超微结构的变化。结果:沙美特罗氟替卡松可提高患者肺功能(P<0.05),并且可降低COPD患者TNF-α的浓度(P<0.05),提高COPD患者线粒体氧化磷酸化酶复合体Ⅰ、Ⅱ、Ⅲ的活性,同时可修复COPD患者单核细胞的超微结构。结论:沙美特罗氟替卡松对抗COPD患者成肌细胞线粒体氧化磷酸化功能障碍的机制可能与其降低体内TNF-α的浓度有关。
Objective:To investigate the mechanism of salmeterol fluticasone against myoblast mitochondrial oxidative phosphorylation function obstacle of patients with COPD.Methods:100 patients with COPD in stabe phase were included in this study, and had the 1.5 years follow-up, after the follow-up, 44 cases having the consistent use of salmeterol fluticasone as observation group, and the remaining 56 cases as control group, 50 cases of healthy physical examination as the healthy group. Three groups of lung function, peripheral blood tumor necrosis factor(TNF-) concentration, monocyte mitochondrial oxidative phosphorylation complex expression changes and three groups of monocyte morphology ultrastructural changes were detected.Results:Salmeterol fluticasone can improve lung function(P<0.05), reduce the concentration of TNF-in COPD patients(P<0.05), increase the activity of mitochondrial oxidative phosphorylase complex I, II, III in COPD patients and repair the ultrastructure of monocytes in patients with COPD.Conclusion:The mechanism of salmeterol fluticasone against mitochondrial oxidative phosphorylation dysfunction in myoblasts of COPD patients may be related to the reduction of TNF-concentration in vivo.
Objective:To investigate the mechanism of salmeterol fluticasone against myoblast mitochondrial oxidative phosphorylation function obstacle of patients with COPD.Methods:100 patients with COPD in stabe phase were included in this study, and had the 1.5 years follow-up, after the follow-up, 44 cases having the consistent use of salmeterol fluticasone as observation group, and the remaining 56 cases as control group, 50 cases of healthy physical examination as the healthy group. Three groups of lung function, peripheral blood tumor necrosis factor(TNF-) concentration, monocyte mitochondrial oxidative phosphorylation complex expression changes and three groups of monocyte morphology ultrastructural changes were detected.Results:Salmeterol fluticasone can improve lung function(P<0.05), reduce the concentration of TNF-in COPD patients(P<0.05), increase the activity of mitochondrial oxidative phosphorylase complex I, II, III in COPD patients and repair the ultrastructure of monocytes in patients with COPD.Conclusion:The mechanism of salmeterol fluticasone against mitochondrial oxidative phosphorylation dysfunction in myoblasts of COPD patients may be related to the reduction of TNF-concentration in vivo.
引文
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[3] Jones PW,Quirk FH,Baveystock CM,el al.A self-complele measure of health status for chronic airflow limitation: the St.George's respiratory questionnaire[J].Am Rev Respir Dis,2011,145(11):1321-1327.
[4] Bafadhel M,Umar I,Gupta S,et al.The role of CTscanning in multidimensional phenotyping of COPD[J].Chest,2011,140(3):634-642.
[5] 张昊,周新,张杏怡,等.慢性阻塞性肺病稳定期的下呼吸道细菌定植研究[J].微生物与感染,2010,99(1):102-117.
[6] 王丽,谭焰,谷伟,等.慢性阻塞性肺病缓解期患者血清中TNF-a、IL-6和、IL-8表达的研究[J].临床肺科杂志,2011,16(11):835- 836.
[7] Winder WW. Energy-sensing and signaling by AMP-activated protein kinase in skeletal muscle[J]. J Appl Physiol,2001,91(3):1017-1028.
[8] Bakkar N, Ladner K, Canan BD, et al. IKKalpha and alternative NF-kappaB regulate PGC-1beta to promote oxidative muscle metabolism[J]. J Cell Biol,2012,196(4):497-511.
[9] Wang H, Geng QR, Wang L, et al. Curcumin potentiates antitumor activity of L-asparaginase via inhibition of the AKT signaling pathway in acute lymphoblastic leukemia[J].Leuk Lymphoma,2012,53(7):1376-1382.