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不同脏腑虚损对慢性阻塞性肺疾病患者病情及线粒体功能的影响
Effect on Disease Severity and Mitochondrial Functional Status of Different Viscera Deficiency COPD Patients
投稿时间:2018-02-11  修订日期:2018-03-14
DOI:
中文关键词:  COPD 脏腑虚损 线粒体功能障碍 线粒体膜电位 ROS
英文关键词:COPD, viscera deficiency, mitochondrial dysfunction, mitochondrial membrane potential, ROS
基金项目:国家自然科学基金委员会地区基金(81660740):不同发展速度肺脾虚损慢性阻塞性肺疾病患者血液差异蛋白筛选及相关因子验证研究,负责人:李风森;国家中医药管理局(JDZX2015232):国家中医药管理局国家中医临床研究基地业务建设专项,负责人:李风森。
作者单位
张少华 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 830000 
徐丹 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 830000 
闫雪娇 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 830000 
金晶 1. 新疆医科大学中医学院 乌鲁木齐 8300003. 新疆医科大学附属第一医院中医科 乌鲁木齐 830000 
荆晶 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 830000 
姜敏 1. 新疆医科大学中医学院 乌鲁木齐 8300004. 新疆医科大学附属中医医院呼吸病理生理实验室 乌鲁木齐 830000 
李争 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 830000 
高振 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 830000 
李风森 1. 新疆医科大学中医学院 乌鲁木齐 8300002. 新疆国家中医临床研究基地COPD研究室 乌鲁木齐 8300005. 新疆医科大学附属中医医院呼吸科 乌鲁木齐 830000 
摘要点击次数: 14
全文下载次数: 17
中文摘要:
      目的:探讨不同脏腑虚损对慢性阻塞性肺疾病(COPD)患者病情及线粒体功能的影响。方法:纳入161例COPD稳定期患者,记录病史按脏腑虚损标准对纳入病例进行中医辨证分型,检测患者肺通气功能,采用COPD评估测试量表(CAT)、呼吸困难量表(m MRC)对患者进行评分、进行6 min步行试验(6MWT);采集患者外周血分离有核细胞用流式细胞术进行线粒体膜电位、细胞内活性氧(ROS)检测;采用SPASS21.0对数据进行统计分析。结果:161例COPD患者中辨证为肺气虚者36例,肺脾气虚者31例,肺肾气虚者50例,肺脾肾虚44例,其中104例完成了线粒体实验。COPD患者的病程在肺脾气虚组最长,肺气虚组最短,4组间差异不具显著性(P=0.503);肺通气功能FVC%在4组间差异不具有显著性(P=0.265);FEV1%在各组间差异具有显著性(P=0.025);CAT 在各组间差异具有显著性(P=0.001),6MWD 在4 组间差异不具显著性(P=0.057),FEV1%、FVC%、6MWT均值在肺脾肾虚组最低,CAT均值在肺脾肾虚组最高。线粒体膜电位(MTP)在肺脾气虚组与肺气虚组、肺肾气虚组比较差异有显著性(P<0.05);细胞内活性氧(ROS)在肺脾气虚组与肺气虚组、肺肾气虚组比较差异有显著性(P<0.01);线粒体膜电位(MTP)在肺脾气虚组明显降低,细胞内活性氧(ROS)在肺脾气虚组明显升高。结论:COPD的防治应重视脏腑虚损在发病中的作用;COPD患者线粒体功能障碍与脾虚有关,推测补脾疗法可能改善线粒体功能障碍。
英文摘要:
      This study was aimed to explore the disease severity and mitochondrial functional status of different visceradeficiency chronic obstructive pulmonary disease (COPD) patients. A total of 161 patients with stable COPD wereenrolled. Disease history was recorded and the viscera deficiency was differentiated according to traditional Chinesemedicine (TCM) syndrome differentiation. Pulmonary ventilation function was measured. Evaluation was given onpatients by CAT and mMRC. A 6-minute walk test (6MWT) was performed. The nucleated cells were isolated fromperipheral blood of patients. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) weredetected by flow cytometry. SPASS21.0 was used to analyze the data. The results showed that among 161 COPD cases, 36cases were diagnosed as lung qi deficiency, 31 cases were diagnosed as lung and spleen qi deficiency, 50 cases werediagnosed as lung and kidney qi deficiency, 44 cases were diagnosed as lung, spleen and kidney deficiency, of which 104 cases completed the mitochondrial experiment. The course of disease in COPD patients was the longest in the lung andspleen qi deficiency group, and the shortest in the lung qi deficiency group. There was no significant difference amongfour groups (P=0.503). There was no significant difference on pulmonary ventilation function FVC% among four groups(P=0.265). There was significant difference on FEV1% among different groups (P=0.025). There was significantdifference on CAT among different groups (P=0.001). There was no significant difference on 6MWD among four groups(P=0.057). The mean values of FEV1%, FVC% and 6MWT were the lowest in the lung, spleen and kidney deficiencygroup; and the mean value of CAT was the highest in the lung, spleen and kidney deficiency group. The mitochondrialmembrane potential in the lung and spleen qi deficiency group had significant difference compared to that of the lung qideficiency group, and the lung and kidney qi deficiency group (P<0.05). The intracellular ROS of the lung and spleen qideficiency group had significant difference compared to that of the lung qi deficiency group, and the lung and kidney qideficiency group (P<0.01). Mitochondrial membrane potential decreased significantly in the lung spleen qi deficiencygroup. And ROS increased significantly in the lung spleen qi deficiency group. It was concluded that the prevention andtreatment of COPD should pay attention to the role of viscera deficiency in the pathogenesis of COPD. Mitochondrialdysfunction is associated with spleen deficiency in patients with COPD, which suggests that invigorating spleen mayimprove mitochondrial dysfunction.
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