不同程度脏腑虚损哮喘患者血浆左旋精氨酸和不对称二甲基精氨酸水平以及肺功能的研究
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摘要
目的探讨不同程度脏腑虚损哮喘患者肺功能、血浆左旋精氨酸(L-Arg)及不对称二甲基精氨酸(ADMA)的水平。方法将122例支气管哮喘急性发作期患者作为哮喘组,其中肺气虚者47例、肺脾气虚者39例、肺脾肾虚者36例,并将44例健康正常人作为正常对照组。采用高效液相联合质谱法检测所有研究对象血浆L-Arg及ADMA水平,并对哮喘患者进行肺功能测定。结果哮喘组血浆L-Arg水平及L-Arg/ADMA比值均低于正常对照组(均P <0. 05)。各脏腑虚损组的血浆L-Arg水平、L-Arg/ADMA比值亦均低于正常对照组(均P <0. 05),但不同脏腑虚损组间上述指标差异无统计学意义(均P> 0. 05)。肺气虚组、肺脾气虚组、肺脾肾虚组患者1 s用力呼气容积、1 s用力呼气容积/用力肺活量的比值、呼气流量峰值均依次降低(均P <0. 05)。结论哮喘患者机体均存在精氨酸代谢紊乱,这可能是引起哮喘患者线粒体呼吸链损伤的主要原因,但不同程度脏腑虚损哮喘患者精氨酸代谢水平无差异。哮喘患者肺功能变化与脏腑虚损发展趋势具有一致性。
Objective To explore the lung function and plasma L-arginine( L-Arg) and asymmetric dimethylarginine( ADMA) levels in asthmatic patients with different degrees of zang-fu viscera deficiency. Methods A total of122 patients with acute attack of bronchial asthma were selected as asthma group,including 47 patients with lung qi-deficiency,39 patients with lung and spleen qi-deficiency,and 36 patients with lung,spleen and kidney qi-deficiency,moreover,another healthy individuals were enrolled as normal control group. Plasma L-Arg and ADMA levels of all the subjects were detected by high performance liquid chromatography combined with mass spectrometry,and lung function detection was performed in asthmatic patients. Results The plasma L-Arg level and L-Arg/ADMA ratio in the asthma group were lower than those in the normal control group( all P < 0. 05). The plasma L-Arg level and L-Arg/ADMA ratio in each viscera deficiency group were also lower than those in the normal control group( all P < 0. 05),but no statistically significant differences were found in the indices above among various zang-fu viscera deficiency groups( all P > 0. 05). Forced expiratory volume in one second,ratio of forced expiratory volume in one second to forced vital capacity,and peak expiratory flow decreased in the order of the lung qi-deficiency group,the lung and spleen qi-deficiency group and the lung,spleen and kidney qi-deficiency group( all P < 0. 05). Conclusion Arginine metabolism disorder exists in asthmatic patients,which may be a primary cause leading to mitochondrial respiratory chain injury in asthmatic patients,but there was no significant difference in arginine metabolism level among asthmatic patients with different degrees of zang-fu viscera deficiency. Changes in lung function are consistent with developmental trend of zang-fu viscera deficiency in asthmatic patients.
Objective To explore the lung function and plasma L-arginine( L-Arg) and asymmetric dimethylarginine( ADMA) levels in asthmatic patients with different degrees of zang-fu viscera deficiency. Methods A total of122 patients with acute attack of bronchial asthma were selected as asthma group,including 47 patients with lung qi-deficiency,39 patients with lung and spleen qi-deficiency,and 36 patients with lung,spleen and kidney qi-deficiency,moreover,another healthy individuals were enrolled as normal control group. Plasma L-Arg and ADMA levels of all the subjects were detected by high performance liquid chromatography combined with mass spectrometry,and lung function detection was performed in asthmatic patients. Results The plasma L-Arg level and L-Arg/ADMA ratio in the asthma group were lower than those in the normal control group( all P < 0. 05). The plasma L-Arg level and L-Arg/ADMA ratio in each viscera deficiency group were also lower than those in the normal control group( all P < 0. 05),but no statistically significant differences were found in the indices above among various zang-fu viscera deficiency groups( all P > 0. 05). Forced expiratory volume in one second,ratio of forced expiratory volume in one second to forced vital capacity,and peak expiratory flow decreased in the order of the lung qi-deficiency group,the lung and spleen qi-deficiency group and the lung,spleen and kidney qi-deficiency group( all P < 0. 05). Conclusion Arginine metabolism disorder exists in asthmatic patients,which may be a primary cause leading to mitochondrial respiratory chain injury in asthmatic patients,but there was no significant difference in arginine metabolism level among asthmatic patients with different degrees of zang-fu viscera deficiency. Changes in lung function are consistent with developmental trend of zang-fu viscera deficiency in asthmatic patients.
引文
[1]张晓岩,林江涛.支气管哮喘的流行病学及发病危险因素[J].中华结核和呼吸杂志,2007,30(7):538-541.
[2]夏晶. DDAH2/ADMA通路在高糖诱导内皮祖细胞线粒体功能障碍中的作用及机制[D].长沙:中南大学,2013.
[3] Li M,Shang YX. Ultrastructural changes in rat airway epithelium in asthmatic airway remodeling[J]. Pathol Res Pract,2014,210(12):1 038-1 042.
[4] Aguilera-Aguirre L,Bacsi A,Saavedra-Molina A,et al. Mitochondrial dysfunction increases allergic airway inflammation[J]. J Immunol,2009,183(8):5 379-5 387.
[5] Aravamudan B,Thompson MA,Pabelick CM,et al. Mitochondria in lung diseases[J]. Expert Rev Respir Med,2013,7(6):631-646.
[6]王小平,韩学海,杨福愉.脱血红素细胞色素c的68~88肽段在插膜及与线粒体结合中具有关键作用[J].中国科学C辑(生命科学),2002,32(4):334-341.
[7] Ramuschkat M,Appelbaum S,Atzler D,et al. ADMA,subclinical changes and atrial fibrillation in the general population[J]. Int J Cardiol,2015,203:640-646.
[8] Németh B,Kiss I,Péter I,et al. Monitoring of L-arginine and endogenous dimethylarginines in survivor septic patients-a pilot study[J]. In Vivo,2016,30(5):663-669.
[9] Zinellu A,Fois AG,Sotgia S,et al. Arginines plasma concentration and oxidative stress in mild to moderate COPD[J].PLo S One,2016,11(8):e0160237.
[10] Snyder CM,Shroff EH,Liu J,et al. Nitric oxide induces cell death by regulating anti-apoptotic BCL-2 family members[J].PLo S One,2009,4(9):e7059.
[11]中华医学会呼吸病学分会哮喘学组.支气管哮喘防治指南(2016年版)[J].中华结核和呼吸杂志,2016,39(9):675-697.
[12]张伯臾.中医内科学[M].上海:上海科学技术出版社,1985:59.
[13]朱文峰.中医诊断学[M].上海:上海科学技术出版社,1995:145,164.
[14]晁恩祥,孙增涛,刘恩顺.支气管哮喘中医诊疗专家共识(2012)[J].中医杂志,2013,54(7):627-629.
[15] lwasaki H. Activities of asymmetric dimethylarginine-related enzymes in white adipose tissue are associated with circulating lipid biomarkers[J]. Diabetol Metab Syndr,2012,4(1):17.
[16] Alpoim PN,Sousa LP,Mota AP,et al. Asymmetric Dimethylarginine(ADMA)in cardiovascular and renal disease[J].Clin Chim Acta,2015,440:36-39.
[17] Maas R. Pharmacotherapies and their influence on asymmetric dimethylargine(ADMA)[J]. Vasc Med,2005,10(Suppl 1):S49-S57.
[18]呼晓雷,周继鹏,陈小平. AGXT2与ADMA代谢及心脑血管疾病的研究进展[J].中国药理学通报,205,31(5):601-605.
[19]海春霞.非对称性二甲基精氨酸抑制2型糖尿病大鼠心肌线粒体生物合成与ATP生成及其机制[D].长沙:中南大学,2009.
[20]张如.非对称性二甲基精氨酸在老年大鼠心肌细胞衰老中的作用及其机制[D].长沙:中南大学,2010.
[21]李凡,高芬.一氧化氮合酶在高原地区支气管哮喘发病机制中的作用[J].高原医学杂志,2008,39(2):8-10.
[22]王至婉,李建生,余学庆,等.支气管哮喘不同时期证候演变规律的临床调查研究[J].北京中医药大学学报,2016,39(2):136-139.
[23]朱金凤.支气管哮喘的中医辨治思维与方法研究[J].中国中医基础医学杂志,2016,22(2):284-286.
[24]张文瑞,杨爽,王盛隆,等.支气管哮喘中医证候及治疗研究[J].吉林中医药,2015,35(5):463-466.
[2]夏晶. DDAH2/ADMA通路在高糖诱导内皮祖细胞线粒体功能障碍中的作用及机制[D].长沙:中南大学,2013.
[3] Li M,Shang YX. Ultrastructural changes in rat airway epithelium in asthmatic airway remodeling[J]. Pathol Res Pract,2014,210(12):1 038-1 042.
[4] Aguilera-Aguirre L,Bacsi A,Saavedra-Molina A,et al. Mitochondrial dysfunction increases allergic airway inflammation[J]. J Immunol,2009,183(8):5 379-5 387.
[5] Aravamudan B,Thompson MA,Pabelick CM,et al. Mitochondria in lung diseases[J]. Expert Rev Respir Med,2013,7(6):631-646.
[6]王小平,韩学海,杨福愉.脱血红素细胞色素c的68~88肽段在插膜及与线粒体结合中具有关键作用[J].中国科学C辑(生命科学),2002,32(4):334-341.
[7] Ramuschkat M,Appelbaum S,Atzler D,et al. ADMA,subclinical changes and atrial fibrillation in the general population[J]. Int J Cardiol,2015,203:640-646.
[8] Németh B,Kiss I,Péter I,et al. Monitoring of L-arginine and endogenous dimethylarginines in survivor septic patients-a pilot study[J]. In Vivo,2016,30(5):663-669.
[9] Zinellu A,Fois AG,Sotgia S,et al. Arginines plasma concentration and oxidative stress in mild to moderate COPD[J].PLo S One,2016,11(8):e0160237.
[10] Snyder CM,Shroff EH,Liu J,et al. Nitric oxide induces cell death by regulating anti-apoptotic BCL-2 family members[J].PLo S One,2009,4(9):e7059.
[11]中华医学会呼吸病学分会哮喘学组.支气管哮喘防治指南(2016年版)[J].中华结核和呼吸杂志,2016,39(9):675-697.
[12]张伯臾.中医内科学[M].上海:上海科学技术出版社,1985:59.
[13]朱文峰.中医诊断学[M].上海:上海科学技术出版社,1995:145,164.
[14]晁恩祥,孙增涛,刘恩顺.支气管哮喘中医诊疗专家共识(2012)[J].中医杂志,2013,54(7):627-629.
[15] lwasaki H. Activities of asymmetric dimethylarginine-related enzymes in white adipose tissue are associated with circulating lipid biomarkers[J]. Diabetol Metab Syndr,2012,4(1):17.
[16] Alpoim PN,Sousa LP,Mota AP,et al. Asymmetric Dimethylarginine(ADMA)in cardiovascular and renal disease[J].Clin Chim Acta,2015,440:36-39.
[17] Maas R. Pharmacotherapies and their influence on asymmetric dimethylargine(ADMA)[J]. Vasc Med,2005,10(Suppl 1):S49-S57.
[18]呼晓雷,周继鹏,陈小平. AGXT2与ADMA代谢及心脑血管疾病的研究进展[J].中国药理学通报,205,31(5):601-605.
[19]海春霞.非对称性二甲基精氨酸抑制2型糖尿病大鼠心肌线粒体生物合成与ATP生成及其机制[D].长沙:中南大学,2009.
[20]张如.非对称性二甲基精氨酸在老年大鼠心肌细胞衰老中的作用及其机制[D].长沙:中南大学,2010.
[21]李凡,高芬.一氧化氮合酶在高原地区支气管哮喘发病机制中的作用[J].高原医学杂志,2008,39(2):8-10.
[22]王至婉,李建生,余学庆,等.支气管哮喘不同时期证候演变规律的临床调查研究[J].北京中医药大学学报,2016,39(2):136-139.
[23]朱金凤.支气管哮喘的中医辨治思维与方法研究[J].中国中医基础医学杂志,2016,22(2):284-286.
[24]张文瑞,杨爽,王盛隆,等.支气管哮喘中医证候及治疗研究[J].吉林中医药,2015,35(5):463-466.