Is oxidative stress associated with disease severity, pulmonary function and metabolic syndrome in chronic obstructive pulmonary disease?

Sepúlveda-Loyola, Walter; Machado, Felipe; Castro, Larissa Araújo de; Baltus, Thiago Hissnauer Leal; Morelli, Nayara Rampazzo; Bonifácio, Kamila Landucci; Morita, A.A.; Michelin, A.P.; Barbosa, Décio Sabbatini; Probst, Vanessa Suziane

doi:10.1016/j.rceng.2019.04.009

Cited by 5 publications

(15 citation statements)

References 36 publications

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“…One study [28] was excluded because it included the same population as another study [29]. Finally, 12 studies were identified [13,14,[28][29][30][31][32][33][34][35][36][37]. Table 1 shows a summary of the included studies.…”

Section: Resultsmentioning

confidence: 99%

“…Arylesterase activity showed a similar trend (Figure 5). Some studies [14,28,[32][33][34][35] reported the HDL-cholesterol (HDL-C) level in addition to PON1 activity. One study that included patients with severe COPD showed low levels of HDL-C [14], while another study showed high levels of HDL-C [28].…”

Section: Resultsmentioning

confidence: 99%

“…Some studies [14,28,[32][33][34][35] reported the HDL-cholesterol (HDL-C) level in addition to PON1 activity. One study that included patients with severe COPD showed low levels of HDL-C [14], while another study showed high levels of HDL-C [28]. In three other studies that mainly included patients with non-severe COPD, the HDL-C levels were high In subgroup analyses by the severity of COPD, paraoxonase activity was found to be significantly low in studies that mainly included patients with non-severe COPD (SMD, −1.46; 95% CI, −2.03 to −0.89; I 2 = 91%) and, in contrast, was slightly but significantly higher in studies that included patients with severe COPD (SMD, 0.33; 95% CI, 0.02 to 0.64; I 2 = 64%) in comparison to healthy controls (Figure 4).…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

“…One study that included patients with severe COPD showed low levels of HDL-C [14], while another study showed high levels of HDL-C [28]. In three other studies that mainly included patients with non-severe COPD, the HDL-C levels were high Some studies [14,28,[32][33][34][35] reported the HDL-cholesterol (HDL-C) level in addition to PON1 activity. One study that included patients with severe COPD showed low levels of HDL-C [14], while another study showed high levels of HDL-C [28].…”

Section: Resultsmentioning

confidence: 99%

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Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

2021

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Oxidative stress is a driving factor in the pathophysiology of chronic obstructive pulmonary disease (COPD). While paraoxonase 1 (PON1) is an antioxidant enzyme and a potential biomarker of this disease, data regarding the status of PON-1 in COPD are inconclusive. In this regard, to shed light on this issue, we performed a meta-analysis of data on PON1 activity in COPD. Electronic databases (MEDLINE, Embase and CENTRAL) were searched for available studies on PON1 activity in patients with stable COPD published before October 2021. A meta-analysis was performed using random-effects models. Twelve studies (12 studies on paraoxonase and three on arylesterase) were identified. Patients with COPD had lower levels of paraoxonase activity (standard mean difference [SMD] −0.77, 95% confidence interval [CI] −1.35 to −0.18) and arylesterase activity (SMD −1.15, 95% CI −1.95 to −0.36) in comparison to healthy controls. In subgroup analyses, paraoxonase activity was lower in patients of studies as consisted of mainly non-severe COPD (SMD −1.42, 95% CI −2.04 to −0.79) and, by contrast, slightly higher in patients of studies including severe COPD (SMD 0.33, 95% CI 0.02 to 0.64) in comparison to healthy controls. Arylesterase activity showed a similar trend. Overall, PON1 activity was lower in patients with COPD, suggesting that PON1-related antioxidant defense is impaired in COPD. Future studies are warranted.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

2021

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Glycyl‐l‐histidyl‐l‐lysine‐Cu²⁺ rescues cigarette smoking‐induced skeletal muscle dysfunction via a sirtuin 1‐dependent pathway

Deng

Zhang

Yan

et al. 2023

J cachexia sarcopenia muscle

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Background Skeletal muscle dysfunction is an important co‐morbidity in patients with chronic obstructive pulmonary disease (COPD) and is significantly associated with increased mortality. Oxidative stress has been demonstrated an important trigger for COPD‐related skeletal muscle dysfunction. Glycine‐histidine‐lysine (GHK) is an active tripeptide, which is a normal component of human plasma, saliva, and urine; promotes tissue regeneration; and acts as an anti‐inflammatory and antioxidant properties. The purpose of this study was to determine whether GHK is involved in COPD‐related skeletal muscle dysfunction. Methods The plasma GHK level in patients with COPD (n = 9) and age‐paired healthy subjects (n = 11) were detected using reversed‐phase high‐performance liquid chromatography. The complex GHK with Cu (GHK‐Cu) was used in in vitro (C2C12 myotubes) and in vivo experiments (cigarette smoking [CS]‐exposure mouse model) to explore the involvement of GHK in CS‐induced skeletal muscle dysfunction. Results Compared with healthy control, plasma GHK levels were decreased in patients with COPD (70.27 ± 38.87 ng/mL vs. 133.0 ± 54.54 ng/mL, P = 0.009). And plasma GHK levels in patients with COPD were associated with pectoralis muscle area (R = 0.684, P = 0.042), inflammatory factor TNF‐α (R = −0.696, P = 0.037), and antioxidative stress factor SOD2 (R = 0.721, P = 0.029). GHK‐Cu was found to rescue CSE‐induced skeletal muscle dysfunction in C2C12 myotubes, as evidenced by increased expression of myosin heavy chain, reduced expression of MuRF1 and atrogin‐1, elevated mitochondrial content, and enhanced resistance to oxidative stress. In CS‐induced muscle dysfunction C57BL/6 mice, GHK‐Cu treatment (0.2 and 2 mg/kg) reduces CS‐induced muscle mass loss (skeletal muscle weight (1.19 ± 0.09% vs. 1.29 ± 0.06%, 1.40 ± 0.05%; P < 0.05) and muscle cross‐sectional area elevated (1055 ± 552.4 μm2 vs. 1797 ± 620.9 μm2, 2252 ± 534.0 μm2; P < 0.001), and also rescues CS‐induced muscle weakness, indicated by improved grip strength (175.5 ± 36.15 g vs. 257.6 ± 37.98 g, 339.1 ± 72.22 g; P < 0.01). Mechanistically, GHK‐Cu directly binds and activates SIRT1(the binding energy was −6.1 kcal/mol). Through activating SIRT1 deacetylation, GHK‐Cu inhibits FoxO3a transcriptional activity to reduce protein degradation, deacetylates Nrf2 and contribute to its action of reducing oxidative stress by generation of anti‐oxidant enzymes, increases PGC‐1α expression to promote mitochondrial function. Finally, GHK‐Cu could protect mice against CS‐induced skeletal muscle dysfunction via SIRT1. Conclusions Plasma glycyl‐l‐histidyl‐l‐lysine level in patients with chronic obstructive pulmonary disease was significantly decreased and was significantly associated with skeletal muscle mass. Exogenous administration of glycyl‐l‐histidyl‐l‐lysine‐Cu2+ could protect against cigarette smoking‐induced skeletal muscle dysfunction via sirtuin 1.

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Chronic obstructive pulmonary disease and metabolic syndrome: traveling with bad companies

Andreu

Rodríguez

2019

Revista Clínica Española (English Edition)

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Is oxidative stress associated with disease severity, pulmonary function and metabolic syndrome in chronic obstructive pulmonary disease?

Cited by 5 publications

References 36 publications

Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

Glycyl‐l‐histidyl‐l‐lysine‐Cu²⁺ rescues cigarette smoking‐induced skeletal muscle dysfunction via a sirtuin 1‐dependent pathway

Chronic obstructive pulmonary disease and metabolic syndrome: traveling with bad companies

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Is oxidative stress associated with disease severity, pulmonary function and metabolic syndrome in chronic obstructive pulmonary disease?

Cited by 5 publications

References 36 publications

Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

Glycyl‐l‐histidyl‐l‐lysine‐Cu2+ rescues cigarette smoking‐induced skeletal muscle dysfunction via a sirtuin 1‐dependent pathway

Chronic obstructive pulmonary disease and metabolic syndrome: traveling with bad companies

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Glycyl‐l‐histidyl‐l‐lysine‐Cu²⁺ rescues cigarette smoking‐induced skeletal muscle dysfunction via a sirtuin 1‐dependent pathway