Bufei Jianpi granules decrease skeletal muscular cell apoptosis via improving mitochondrial dysfunction in rats with chronic obstructive pulmonary disease

2017 ◽  
Author(s):  
Jing Mao ◽  
Ya Li ◽  
Qingqing Bian ◽  
Junzi Li ◽  
Lanxi Zhang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mitochondrial Dysfunction ◽  
Pulmonary Disease ◽  
Cell Apoptosis ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals Bufei Jianpi Granules Reduce Quadriceps Muscular Cell Apoptosis by Improving Mitochondrial Function in Rats with Chronic Obstructive Pulmonary Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Mao ◽  
Ya Li ◽  
Suyun Li ◽  
Jiansheng Li ◽  
Yange Tian ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Pulmonary Disease ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Smoke Inhalation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients

Background. Cell apoptosis is an important mechanism underlying skeletal muscle dysfunction in chronic obstructive pulmonary disease (COPD) patients, and mitochondrial dysfunction is recognized as a central aspect contributing to skeletal muscle deterioration. Bufei Jianpi granules have been confirmed effective for improving motor function in COPD patients, but the specific mechanism for this improved function remains unknown. This study explored the mechanisms by which Bufei Jianpi granules improve cell apoptosis and mitochondrial dysfunction in COPD. Methods. Sprague-Dawley rats were randomized into control, model, Bufei Jianpi, and aminophylline groups. A stable COPD rat model was induced with respective repeated cigarette smoke inhalation and intragastric bacterial infection, and rats were sacrificed after 20 weeks; the quadriceps muscle was harvested from each rat. Skeletal muscle mitochondria were extracted for measurements of mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore openings (mPTPs). ATP levels were determined with a firefly luciferase-based ATP assay kit. The rates of cell apoptosis were determined by the transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) method. Cyto C and caspase-3 mRNA and protein levels were measured by qPCR and western blotting. Results. ATP, MMP, and mPTPs were markedly decreased in COPD rats, while cell apoptosis, caspase-3, and Cyto C were increased (P<0.01). All aforementioned parameters were improved in treatment groups (P<0.05). ATP, MMP, and mPTPs were significantly higher in the Bufei Jianpi group than in the aminophylline group, while cell apoptosis, caspase-3, and Cyto C were lower (P<0.05). Conclusions. Bufei Jianpi granules can inhibit mitochondrial dysfunction and cell apoptosis in peripheral muscles, which might be the mechanism involved in improving skeletal muscle function in COPD patients.

scholarly journals Development of secondary mitochondrial dysfunction of mononuclear blood leukocytes in patients with chronic obstructive pulmonary disease and chronic bronchitis

2018 ◽  
Vol 99 (5) ◽  
pp. 741-747
Author(s):  
E S Bel’skikh ◽  
O M Uryas’ev ◽  
V I Zvyagina ◽  
S V Faletrova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mitochondrial Dysfunction ◽  
Chronic Bronchitis ◽  
Pulmonary Disease ◽  
Oxidative Modification ◽  
Mononuclear Leukocytes ◽  
Chronic Obstructive ◽  
Adaptive Potential ◽  
Obstructive Pulmonary Disease ◽  
Oxidative Modification Of Proteins

Aim. To study the indicators of energy metabolism and oxidative stress in mononuclear leukocytes of peripheral blood and to assess the possibility of mitochondrial dysfunction development in chronic obstructive pulmonary disease and chronic bronchitis. Methods. The study included 50 patients aged 40 to 75 years with chronic obstructive pulmonary disease (COPD) or chronic bronchitis. The first group included 13 patients with chronic bronchitis. In accordance with the GOLD spirometric classification, the second and third groups included patients with COPD of moderate severity (COPD 2) (n=17) and severe COPD (COPD 3) (n=20) respectively. In the isolated mononuclear leukocytes, the activity of superoxide dismutase (SOD), succinate dehydrogenase (SDH) and concentration of succinate were determined, a complex evaluation of oxidative modification of proteins was performed. Results. Patients with chronic bronchitis compared to patients with COPD 2 and COPD 3 were found to have in mononuclear leukocytes higher activity of SOD by 3.38 times (p=0.0025) and 3.15 times (p=0.0058), higher activity of SDH by 4.55 times (p=0.0281) and 2.5 times (p=0.0263) and higher succinate concentration by 2.05 (p=0.0133) and 1.89 (p=0.005) times respectively. The level of spontaneously oxidized modified proteins in the group of patients with chronic bronchitis decreased by 2.45 (p=0.0176) and 2.94 (p=0.0168) times compared to the patients of groups 2 and 3, respectively There was a decrease in the reserve-adaptive potential of oxidative modification of proteins in COPD in the form of an increase of the ratio of spontaneously oxidized-modified proteins to metal-induced oxidized proteins by 1.58 times (p=0.0301) between groups 1 and 2, and by 1.44 times between groups 2 and 3 (p=0.0446). Conclusion. In mononuclear leukocytes of COPD patients, secondary mitochondrial dysfunction is observed accompanied by significant oxidative damage of lymphocytes and monocytes. Patients with severe COPD compared to patients with COPD of moderate severity have less reserve-adaptive potential for the oxidative modification of mononuclear leukocyte proteins, which probably reflects a more severe course of the disease.

scholarly journals The fatty acid composition of the mitochondrial membranes of platelets in chronic obstructive pulmonary disease.

2018 ◽  
Vol 96 (4) ◽  
pp. 343-347
Author(s):  
Y. K. Denisenko ◽  
T. P. Novgorodtseva ◽  
T. I. Vitkina ◽  
M. V. Antonyuk ◽  
Nataliia V. Bocharova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Fatty Acids ◽  
Mitochondrial Dysfunction ◽  
Chronic Bronchitis ◽  
Pulmonary Disease ◽  
Blood Cells ◽  
Transport Systems ◽  
Chronic Obstructive ◽  
Mitochondrial Membranes ◽  
Obstructive Pulmonary Disease

Objective: to study the composition of fatty acids (FA) and mitochondrial membrane potential (MMР) of blood cells in patients with chronic bronchitis (CB) and chronic obstructive pulmonary disease (COPD); to establish the role of the Mitochondrial dysfunction in the formation of respiratory diseases. Material and methods. The study involved 26 patients with chronic bronchitis, 27 - with mild COPD, 21 - with moderate COPD steady flow, 29 healthy people. MMР leukocytes was assessed by flow cytometry. The composition of the FA mitochondrial membranes was studied by gas-liquid chromatography. Results and discussion. With the worsening of the disease (moderate COPD) increases the number of white blood cells with reduced MMP, appears deficit of the saturated, monoenic (14: 0, 16: 0, 18: 0) and n-3 polyunsaturated fatty acids (18: 3n-3 20: 5n-3, 22: 5n-3, 22: 6n-3) in the membrane of the mitochondria. Identified imbalance in the composition of fatty acids verifies the changes in the physicochemical properties of subcellular membrane malfunction membrane transport systems, enzymes and receptors, processes of oxidative phosphorylation. Conclusion: The imbalance in the composition of the LCD mitochondrial membranes lead to the development of mitochondrial dysfunction and the formation of cell hypoxia.

scholarly journals Quadriceps miR-542-3p and -5p are elevated in COPD and reduce function by inhibiting ribosomal and protein synthesis

2019 ◽  
Vol 126 (6) ◽  
pp. 1514-1524 ◽  
Author(s):  
Roser Farre-Garros ◽  
Jen Y. Lee ◽  
S. Amanda Natanek ◽  
Martin Connolly ◽  
Avan A. Sayer ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Protein Synthesis ◽  
Mitochondrial Dysfunction ◽  
Pulmonary Disease ◽  
Physical Performance ◽  
Quadriceps Muscle ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients

Reduced physical performance reduces quality of life in patients with chronic obstructive pulmonary disease (COPD). Impaired physical performance is, in part, a consequence of reduced muscle mass and function, which is accompanied by mitochondrial dysfunction. We recently showed that miR-542-3p and miR-542-5p were elevated in a small cohort of COPD patients and more markedly in critical care patients. In mice, these microRNAs (miRNAs) promoted mitochondrial dysfunction suggesting that they would affect physical performance in patients with COPD, but we did not explore the association of these miRNAs with disease severity or physical performance further. We therefore quantified miR-542-3p/5p and mitochondrial rRNA expression in RNA extracted from quadriceps muscle of patients with COPD and determined their association with physical performance. As miR-542-3p inhibits ribosomal protein synthesis its ability to inhibit protein synthesis was also determined in vitro. Both miR-542-3p expression and -5p expression were elevated in patients with COPD (5-fold P < 0.001) and the degree of elevation associated with impaired lung function (transfer capacity of the lung for CO in % and forced expiratory volume in 1 s in %) and physical performance (6-min walk distance in %). In COPD patients, the ratio of 12S rRNA to 16S rRNA was suppressed suggesting mitochondrial ribosomal stress and mitochondrial dysfunction and miR-542-3p/5p expression was inversely associated with mitochondrial gene expression and positively associated with p53 activity. miR-542-3p suppressed RPS23 expression and maximal protein synthesis in vitro. Our data show that miR-542-3p and -5p expression is elevated in COPD patients and may suppress physical performance at least in part by inhibiting mitochondrial and cytoplasmic ribosome synthesis and suppressing protein synthesis. NEW & NOTEWORTHY miR-542-3p and -5p are elevated in the quadriceps muscle of patients with chronic obstructive pulmonary disease (COPD) in proportion to the severity of their lung disease. These microRNAs inhibit mitochondrial and cytoplasmic protein synthesis suggesting that they contribute to impaired exercise performance in COPD.

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