Physical exercise is effective in preventing cigarette smoke-induced pulmonary oxidative response in mice

Nesi, Renata Tiscoski; Souza, Priscila Soares de; Santos, Giulia P.; Thirupathi, Anand; Menegali, Bruno Thizon; Silveira, Paulo César Lock; Silva, Luciano Acordi da; Valença, Samuel Santos; Pinho, Ricardo A.

doi:10.2147/copd.s93958

Cited by 27 publications

(22 citation statements)

References 42 publications

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“…It is widely accepted that cigarette smoke induces chronic pulmonary inflammation, which can affect not only the airways causing bronchitis but also the distal region of the lungs, contributing to the development of lung parenchyma [ 4 , 11 ]. As a potent proinflammatory agent, cigarette smoke activates the production of different proinflammatory cytokines, such as IL-1 β , IL-6, IL-8, IL-17, and TNF- α , which present a key role in both pulmonary inflammatory and structural alterations [ 12 , 13 ].…”

Section: Discussionmentioning

confidence: 99%

Exercise Inhibits the Effects of Smoke‐Induced COPD Involving Modulation of STAT3

Brandão-Rangel

Bachi

Oliveira-Júnior

et al. 2017

Oxidative Medicine and Cellular Longevity

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Purpose Evaluate the participation of STAT3 in the effects of aerobic exercise (AE) in a model of smoke-induced COPD. Methods C57Bl/6 male mice were divided into control, Exe, COPD, and COPD+Exe groups. Smoke were administered during 90 days. Treadmill aerobic training begun on day 61 until day 90. Pulmonary inflammation, systemic inflammation, the level of lung emphysema, and the airway remodeling were evaluated. Analysis of integral and phosphorylated expression of STAT3 by airway epithelial cells, peribronchial leukocytes, and parenchymal leukocytes was performed. Results AE inhibited smoke-induced accumulation of total cells (p < 0.001), lymphocytes (p < 0.001), and neutrophils (p < 0.001) in BAL, as well as BAL levels of IL-1β (p < 0.001), CXCL1 (p < 0.001), IL-17 (p < 0.001), and TNF-α (p < 0.05), while increased the levels of IL-10 (p < 0.001). AE also inhibited smoke-induced increases in total leukocytes (p < 0.001), neutrophils (p < 0.05), lymphocytes (p < 0.001), and monocytes (p < 0.01) in blood, as well as serum levels of IL-1β (p < 0.01), CXCL1 (p < 0.01), IL-17 (p < 0.05), and TNF-α (p < 0.01), while increased the levels of IL-10 (p < 0.001). AE reduced smoke-induced emphysema (p < 0.001) and collagen fiber accumulation in the airways (p < 0.001). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells (p < 0.001), peribronchial leukocytes (p < 0.001), and parenchymal leukocytes (p < 0.001). Conclusions AE reduces smoke-induced COPD phenotype involving STAT3.

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Section: Discussionmentioning

confidence: 99%

Exercise Inhibits the Effects of Smoke‐Induced COPD Involving Modulation of STAT3

Brandão-Rangel

Bachi

Oliveira-Júnior

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…Based on reports that cigarette smoke increases oxidative stress levels in the lung [ 35 , 36 ], we hypothesized that CRO may have similar effects on the human distal lung cells. Therefore, we treated H441 cells with CRO at 0, 2, 8 and 24 h, and intracellular ROS levels were then detected by the dichlorofluorescein assay.…”

Section: Resultsmentioning

confidence: 99%

Novel mechanisms for crotonaldehyde-induced lung edema

Chang

Cui

et al. 2017

Oncotarget

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BackgroundCrotonaldehyde is a highly noxious α,β-unsaturated aldehyde in cigarette smoke that causes edematous acute lung injury.ObjectiveTo understand how crotonaldehyde impairs lung function, we examined its effects on human epithelial sodium channels (ENaC), which are major contributors to alveolar fluid clearance.MethodsWe studied alveolar fluid clearance in C57 mice and ENaC activity was examined in H441 cells. Expression of α- and γ-ENaC was measured at protein and mRNA levels by western blot and real-time PCR, respectively. Intracellular ROS levels were detected by the dichlorofluorescein assay. Heterologous αβγ-ENaC activity was observed in an oocyte model.ResultsOur results showed that crotonaldehyde reduced transalveolar fluid clearance in mice. Furthermore, ENaC activity in H441 cells was inhibited by crotonaldehyde dose-dependently. Expression of α- and γ-subunits of ENaC was decreased at the protein and mRNA level in H441 cells exposed to crotonaldehyde, which was probably mediated by the increase in phosphorylated extracellular signal-regulated protein kinases 1 and 2. ROS levels increased time-dependently in cells exposed to crotonaldehyde. Heterologous αβγ-ENaC activity was rapidly eliminated by crotonaldehyde.ConclusionOur findings suggest that crotonaldehyde causes edematous acute lung injury by eliminating ENaC activity at least partly via facilitating the phosphorylation of extracellular signal-regulated protein kinases 1 and 2 signal molecules. Long-term exposure may decrease the expression of ENaC subunits and damage the cell membrane integrity, as well as increase the levels of cellular ROS products.

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“…As mentioned previously, cigarette smoke is a similar stimulus for producing ROS. In fact, exercised mice exposed to cigarette smoke experienced reduced oxidative damage to lipids and proteins compared to sedentary smoke-exposed counterparts [46]. Alternatively, postprandial oxidative stress is exacerbated in cigarette smokers [47].…”

Section: Discussionmentioning

confidence: 99%

Chronic Marijuana Smoking Does Not Negatively Impact Select Blood Oxidative Stress Biomarkers in Young, Physically Active Men and Women

Butawan¹,

Smith²

2018

Health

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Background: The smoking of Cannabis sativa, the marijuana plant, is increasing in popularity among young adults, even those who may be engaged in regular exercise (i.e., athletes). Research has shown the plant to have antioxidant and analgesic properties, but the effects on oxidative stress are conflicting. The purpose of this study was to measure blood oxidative stress and cardio-metabolic parameters in physically active men and women who regularly smoke marijuana. Methods: A total of 43 marijuana smokers (23 ± 4 years) and 22 non-smokers (24 ± 7 years), who did not smoke tobacco products, participated in this study. Both smokers and non-smokers engaged in regularly exercise, totaling several hours per week (6.4 ± 4.0 and 6.8 ± 4.4, respectively). Smokers reported using marijuana frequently during the week (4.5 ± 2.3 sessions) for a minimum of three consecutive months prior to participating in the study. Blood samples were collected from participants following a 12-hour fast (all food, drink [except water] and smoking) and analyzed for malondialdehyde, advanced oxidation protein products, glucose, cholesterol, and triglycerides. Heart rate and blood pressure was also measured and recorded. Results: No differences of statistical significance were noted for any variable (p > 0.05), with very similar values noted between smokers and non-smokers. Conclusions: In a sample of young, physically active men and women, regular marijuana smoking is not associated with untoward effects on select biomarkers of oxidative stress and cardio-metabolic health. These findings do not suggest that marijuana smoking can be done without harm, as limitations of this study need to be considered.

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Physical exercise is effective in preventing cigarette smoke-induced pulmonary oxidative response in mice

Cited by 27 publications

References 42 publications

Exercise Inhibits the Effects of Smoke‐Induced COPD Involving Modulation of STAT3

Exercise Inhibits the Effects of Smoke‐Induced COPD Involving Modulation of STAT3

Novel mechanisms for crotonaldehyde-induced lung edema

Chronic Marijuana Smoking Does Not Negatively Impact Select Blood Oxidative Stress Biomarkers in Young, Physically Active Men and Women

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