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
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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。
This study was aimed to explore the disease severity and mitochondrial functional status of different viscera deficiency chronic obstructive pulmonary disease(COPD) patients. A total of 161 patients with stable COPD were enrolled. Disease history was recorded and the viscera deficiency was differentiated according to traditional Chinese medicine(TCM) syndrome differentiation. Pulmonary ventilation function was measured. Evaluation was given on patients by CAT and m MRC. A 6-minute walk test(6MWT) was performed. The nucleated cells were isolated from peripheral blood of patients. Mitochondrial membrane potential and intracellular reactive oxygen species(ROS) were detected by flow cytometry. SPASS21.0 was used to analyze the data. The results showed that among 161 COPD cases, 36 cases were diagnosed as lung qi deficiency, 31 cases were diagnosed as lung and spleen qi deficiency, 50 cases were diagnosed 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 and spleen qi deficiency group, and the shortest in the lung qi deficiency group. There was no significant difference among four 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 significant difference 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 deficiency group; and the mean value of CAT was the highest in the lung, spleen and kidney deficiency group. The mitochondrial membrane potential in the lung and spleen qi deficiency group had significant difference compared to that of the lung qi deficiency group, and the lung and kidney qi deficiency group(P<0.05). The intracellular ROS of the lung and spleen qi deficiency group had significant difference compared to that of the lung qi deficiency group, and the lung and kidney qi deficiency group(P<0.01). Mitochondrial membrane potential decreased significantly in the lung spleen qi deficiency group. And ROS increased significantly in the lung spleen qi deficiency group. It was concluded that the prevention and treatment of COPD should pay attention to the role of viscera deficiency in the pathogenesis of COPD. Mitochondrial dysfunction is associated with spleen deficiency in patients with COPD, which suggests that invigorating spleen may improve mitochondrial dysfunction.
This study was aimed to explore the disease severity and mitochondrial functional status of different viscera deficiency chronic obstructive pulmonary disease(COPD) patients. A total of 161 patients with stable COPD were enrolled. Disease history was recorded and the viscera deficiency was differentiated according to traditional Chinese medicine(TCM) syndrome differentiation. Pulmonary ventilation function was measured. Evaluation was given on patients by CAT and m MRC. A 6-minute walk test(6MWT) was performed. The nucleated cells were isolated from peripheral blood of patients. Mitochondrial membrane potential and intracellular reactive oxygen species(ROS) were detected by flow cytometry. SPASS21.0 was used to analyze the data. The results showed that among 161 COPD cases, 36 cases were diagnosed as lung qi deficiency, 31 cases were diagnosed as lung and spleen qi deficiency, 50 cases were diagnosed 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 and spleen qi deficiency group, and the shortest in the lung qi deficiency group. There was no significant difference among four 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 significant difference 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 deficiency group; and the mean value of CAT was the highest in the lung, spleen and kidney deficiency group. The mitochondrial membrane potential in the lung and spleen qi deficiency group had significant difference compared to that of the lung qi deficiency group, and the lung and kidney qi deficiency group(P<0.05). The intracellular ROS of the lung and spleen qi deficiency group had significant difference compared to that of the lung qi deficiency group, and the lung and kidney qi deficiency group(P<0.01). Mitochondrial membrane potential decreased significantly in the lung spleen qi deficiency group. And ROS increased significantly in the lung spleen qi deficiency group. It was concluded that the prevention and treatment of COPD should pay attention to the role of viscera deficiency in the pathogenesis of COPD. Mitochondrial dysfunction is associated with spleen deficiency in patients with COPD, which suggests that invigorating spleen may improve mitochondrial dysfunction.
引文
1 GOLD Committee.Global strategy for the diagnosis,management,and prevention of chronic obstructive pulmonary disease(Revised 2016).www.goldcopd.com.2016.
2 Lacedonia D,Carpagnano G E,Crisetti E,et al.Mitochondrial DNA alteration in obstructive sleep apnea.Respir Res,2015,16(1):47.
3 Pieters N,Koppen G,Smeets K,et al.Decreased mitochondrial DNA content in association with exposure to polycyclic aromatic hydrocarbons in house dust during wintertime:from a population enquiry to cell culture.PLo S One,2013,8(5):e63208.
4 Rowlands D J.Mitochondria dysfunction:A novel therapeutic target in pathological lung remodeling or bystander?Pharmacology&Therapeutics,2016,166:96-105.
5 李建生.正虚积损为慢性阻塞性肺疾病的主要病机.中华中医药杂志,2011,8(26):1710-1713.
6 中华中医药学会.中医内科常见病诊疗指南,中医病症部分.北京:中国中医药出版社,2008:11-13.
7 李建生,李素云,余学庆.慢性阻塞性肺疾病中医诊疗指南(2011版).中医杂志,2012,53(1):80-84.
8 Dodd J W,Hogg L,Nolan J,et al.The COPD assessment test(CAT):response to pulmonary rehabilitation.A multicentre,prospective study.Thorax,2011,66(5):425-429.
9 Mahler D,Wells C.Evaluation of clinical methods for rating dyspnea.Chest,1988,93(3):580-586.
10 American Thoracic Society.ATS statement:guidelines for the six-minute walk test.Am J Respir Crit Care Med,2002,166:111-117.
11 中华医学会呼吸病分会肺功能专业组.肺功能检查指南—肺量计检查.中华结合和呼吸杂志,2014,7(37):481-486.
12 李建生,余学庆,王明航,等.中医治疗慢性阻塞性肺疾病研究的策略与实践.中华中医药杂志,2012,6(27):1607-1612.
13 Carpagnano G E,Lacedonia D,Malerba M,et al.Foschino-Barbaro.Analysis of mitochondrial DNA alteration in new phenotype ACOS.BMC Pulmonary Medicine,2016,16:31.
14 韩磊,李鸣皋,马贵喜,等.血管紧张素-2对内皮细胞和线粒体跨膜电位影响.中国公共卫生,2009,25(1):51.
15 宋晓冬,刘孟安,孙丰润,等.中药胃肠舒对胃肠平滑肌细胞ATP生成的影响.世界华人消化杂志,2007,15(30):3162.
16 刘友章,刘江凯,弓淑珍,等.中医“脾主肌肉”与骨骼肌舒缩运动中能量代谢关系的探讨.江苏中医药,2009,41(4):5.
2 Lacedonia D,Carpagnano G E,Crisetti E,et al.Mitochondrial DNA alteration in obstructive sleep apnea.Respir Res,2015,16(1):47.
3 Pieters N,Koppen G,Smeets K,et al.Decreased mitochondrial DNA content in association with exposure to polycyclic aromatic hydrocarbons in house dust during wintertime:from a population enquiry to cell culture.PLo S One,2013,8(5):e63208.
4 Rowlands D J.Mitochondria dysfunction:A novel therapeutic target in pathological lung remodeling or bystander?Pharmacology&Therapeutics,2016,166:96-105.
5 李建生.正虚积损为慢性阻塞性肺疾病的主要病机.中华中医药杂志,2011,8(26):1710-1713.
6 中华中医药学会.中医内科常见病诊疗指南,中医病症部分.北京:中国中医药出版社,2008:11-13.
7 李建生,李素云,余学庆.慢性阻塞性肺疾病中医诊疗指南(2011版).中医杂志,2012,53(1):80-84.
8 Dodd J W,Hogg L,Nolan J,et al.The COPD assessment test(CAT):response to pulmonary rehabilitation.A multicentre,prospective study.Thorax,2011,66(5):425-429.
9 Mahler D,Wells C.Evaluation of clinical methods for rating dyspnea.Chest,1988,93(3):580-586.
10 American Thoracic Society.ATS statement:guidelines for the six-minute walk test.Am J Respir Crit Care Med,2002,166:111-117.
11 中华医学会呼吸病分会肺功能专业组.肺功能检查指南—肺量计检查.中华结合和呼吸杂志,2014,7(37):481-486.
12 李建生,余学庆,王明航,等.中医治疗慢性阻塞性肺疾病研究的策略与实践.中华中医药杂志,2012,6(27):1607-1612.
13 Carpagnano G E,Lacedonia D,Malerba M,et al.Foschino-Barbaro.Analysis of mitochondrial DNA alteration in new phenotype ACOS.BMC Pulmonary Medicine,2016,16:31.
14 韩磊,李鸣皋,马贵喜,等.血管紧张素-2对内皮细胞和线粒体跨膜电位影响.中国公共卫生,2009,25(1):51.
15 宋晓冬,刘孟安,孙丰润,等.中药胃肠舒对胃肠平滑肌细胞ATP生成的影响.世界华人消化杂志,2007,15(30):3162.
16 刘友章,刘江凯,弓淑珍,等.中医“脾主肌肉”与骨骼肌舒缩运动中能量代谢关系的探讨.江苏中医药,2009,41(4):5.