单核白细胞的琥珀酸及琥珀酸脱氢酶酶作为慢性阻塞性肺疾病患者线粒体快速适应缺氧的标志。
- 作者: Belskikh E.S.1, Uryasiev O.M.1, Zvyagina V.I.1, Faletrova S.V.1
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隶属关系:
- Ryazan State Medical University
- 期: 卷 28, 编号 1 (2020)
- 页面: 13-20
- 栏目: Original study
- URL: https://bakhtiniada.ru/pavlovj/article/view/14376
- DOI: https://doi.org/10.23888/PAVLOVJ202028113-20
- ID: 14376
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目的:研究单核白细胞的琥珀酸浓度和琥珀酸脱氢酶 (SDG) 活性作为慢性阻塞性肺疾病 (COPD) 患者恶化时线粒体快速适应缺氧的标志。
材料与方法:该研究包括58名COPD患者和13名40-75岁的假定健康志愿者。根据GOLD 2018综合评估原则,患者分为B组 (n=18) 、C组 (n=20) 、D组 (n=20) 。患者的年龄、FEV1水平、包/年指数都是可以相比较的。D组患者的低氧血症比其他患者更明显。从血液中分离的单核白细胞中来测定SDG活性和琥珀酸盐的浓度。
结果:根据病情恶化的次数及症状的表现程度分为小组的COPD患者,以单核白细胞线粒体紊乱程度不同为特征。C组单核白细胞中琥珀酸浓度最高 (428 [357;545] nmol/106/毫升 细胞悬液的总体积 (毫升) ,并SDG活性也最高 (64 [56;73] nmol / 分钟*106/毫升 细胞悬液的总体积 (毫升) ,与B组相比 (琥珀酸浓度下降1.43倍,p=0.002;SDG下降1.88倍,p=0.0015) ,而D (琥珀酸浓度下降2.06倍,p<0.0001;SDG下降4.26倍,p<0.0001) 。D组患者对缺氧适应的标志物减少最明显。
结论:COPD患者病情恶化期间少数症状与单核白细胞线粒体快速适应缺氧机制的最高指标相关。患者出现严重症状和频繁病症恶化与线粒体对缺氧 适应机制的最严重破坏有关。
作者简介
Eduard Belskikh
Ryazan State Medical University
编辑信件的主要联系方式.
Email: ed.bels@yandex.ru
ORCID iD: 0000-0003-1803-0542
SPIN 代码: 9350-9360
Scopus 作者 ID: 57195313786
Researcher ID: A-7202-2019
PhD-Student of the Department of Faculty Therapy with the Course of Therapy of the Faculty of Additional Postgraduate Education
俄罗斯联邦, RyazanOleg Uryasiev
Ryazan State Medical University
Email: ed.bels@yandex.ru
ORCID iD: 0000-0001-8693-4696
SPIN 代码: 7903-4609
Researcher ID: S-6270-2016
MD, PhD, Prof., Head of the Department of Faculty Therapy with the Course of Therapy of the Faculty of Additional Postgraduate Education
俄罗斯联邦, RyazanValentina Zvyagina
Ryazan State Medical University
Email: ed.bels@yandex.ru
ORCID iD: 0000-0003-2800-5789
SPIN 代码: 7553-8641
PhD in Biological Science, Associate Professor of the Department of Biological Chemistry with the Clinical Laboratory Diagnostics of Diseases Course of the Faculty of Additional Postgraduate Education
俄罗斯联邦, RyazanSvetlana Faletrova
Ryazan State Medical University
Email: ed.bels@yandex.ru
ORCID iD: 0000-0003-1532-0827
SPIN 代码: 1427-8316
Assistant of the Department of Faculty Therapy with the Course of Therapy of the Faculty of Additional Postgraduate Education
俄罗斯联邦, Ryazan参考
- Barabanova EN. GOLD 2017: what change were made in global strategy of treatment of chronic obstructive pulmo-nary disease and why? Pulʹmono-logiâ. 2017;27(2):274-82. (In Russ). doi:10.18093/ 0869-0189-2017-27-2-274-282
- Nizov AA, Ermachkova AN, Abrosimov VN, et al. Complex assessment of the degree of chronic obstructive pulmo-nary disease COPD severity on out-patient visit. I.P. Pavlov Russian Medical Biological Herald. 2019;27(1):59-65. (In Russ). doi:10.23888/ PAVLOVJ201927159-65
- Nam HS, Izumchenko E, Dasgupta S, et al. Mitochondria in chronic obstructive pulmonary disease and lung cancer: where are we now? Biomarkers in Medicine. 2017;11(6):475-89. doi: 10.2217/bmm-2016-0373
- Agrawal A, Mabalirajan U. Rejuvenating cellular respiration for optimizing respiratory function: targeting mitochon-dria. American Journal of Physiology. Lung Cellular and Molecular Physiology. 2016; 310(2):103-13. doi: 10.1152/ajplung.00320.2015
- Lerner CA, Sundar IK, Rahman I. Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD. International Journal of Biochemistry & Cell Biology. 2016;81(Pt B):294-306. doi: 10.1016/j.biocel.2016.07.026
- Li LA, Lebed'ko OA, Kozlov VK. Assessment of mitochondrial dysfunction in children with community-acquired pneumonia. Far East Medical Journal. 2015;(2):30-6. (In Russ).
- Singh S, Verma SK, Kumar S, et al. Evaluation of Oxidative Stress and Antioxidant Status in Chronic Obstructive Pulmonary Disease. Scandinavian Jour-nal of Immunology. 2017;85(2):130-7. doi:10.1111/ sji.12498
- Lobanova EG, Kondratiyeva EV, Mineyeva EE, et al. The membrane potential of mitochondria of thrombocytes in patients with chronic obstructive disease of lungs. Russian Clinical Laboratory Diagnostics. 2014;59(6):13-6. (In Russ).
- Denisenko YuK, Novgorodtseva TP, Vitkina TI, et al. Mitochondrial dysfunction in chronic obstructive pulmonary disease. Byulleten’ Fiziologii i Patologii Dykhaniya. 2016;(60):28-33. (In Russ). doi: 10.12737/20048
- Lukyanova LD, Kirova YI. Mitochondria-control-led signaling mechanisms of brain protection in hypoxia. Frontiers in Neuroscience. 2015;9:320. doi: 10.3389/fnins.2015.00320
- Belskikh ES, Uryas'ev OM, Zvyagina VI, et al. Investigation of oxidative stress and function of mitochondria in mononuclear leukocytes of blood in patients with chronic bronchitis and with chronic obstructive pulmonary disease. Nauka Molodyh (Eruditio Juvenium). 2018;6(2):203-10. (In Russ). doi: 10.23888/HMJ201862203-210
- Metody biokhimicheskikh issledovaniy: (Lipidnyy i ehnergeticheskiy obmen). Leningrad: Izdatel’stvo Leningrad-skogo gosudarstvennogo universiteta; 1982. (In Russ).
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