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

Brandão-Rangel, Maysa Alves Rodrigues; Bachi, André Luís Lacerda; Oliveira-Júnior, Manoel Carneiro; Abbasi, Asghar; Silva-Rennó, Adriano; Brito, Auriléia Aparecida de; Oliveira, Ana Paula Ligeiro de; Toledo-Arruda, Alessandra Choqueta de; Belvisi, Maria G.

doi:10.1155/2017/6572714

Cited by 13 publications

(4 citation statements)

References 37 publications

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“…In addition, AE modulates several aspects of airway epithelial responses, which have been studied in asthma [18] and COPD [56]. In the present study, we demonstrated for the first time that AE induces IL-10 synthesis by pulmonary leukocytes and airway epithelial cells in mice submitted to PS infection, while leukocyte and epithelial NF-kB expression was reduced.…”

Section: Discussionsupporting

confidence: 60%

Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice

et al. 2018

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Background: Pseudomonas aeruginosa (PS) infection results in severe morbidity and mortality, especially in immune-deficient populations. Aerobic exercise (AE) modulates the immune system, but its effects on the outcomes of pulmonary PS infection in elderly mice are unknown. Methods: BALB/c mice (24 weeks old) were randomized to sedentary, exercise (EX), PS, and PS + EX groups for the acute experimental setting, and PS and PS + EX groups for the chronic setting. Low-intensity AE was performed for 5 weeks, 60 min/day; 24 h after the final AE session, mice were inoculated with 5 × 10⁴ colony-forming units (CFU) of PS, and 24 h and 14 days after PS inoculation, mice were studied. Results: AE inhibited PS colonization (p < 0.001) and lung inflammation (total cells, neutrophils, lymphocytes [p < 0.01] in bronchoalveolar lavage [BAL]), with significant differences in BAL levels of IL-1β (p < 0.001), IL-6 (p < 0.01), CXCL1 (p < 0.001), and TNF-α (p < 0.001), as well as parenchymal neutrophils (p < 0.001). AE increased BAL levels of IL-10 and parenchymal (p < 0.001) and epithelial (p < 0.001) IL-10 expression, while epithelial (p < 0.001) and parenchymal (p < 0.001) NF-κB expression was decreased. AE diminished pulmonary lipid peroxidation (p < 0.001) and increased glutathione peroxidase (p < 0.01). Pre-incubation of BEAS-2B with IL-10 inhibited PS-induced epithelial cell expression of TNF-α (p < 0.05), CD40 (p < 0.01), and dichlorodihydrofluorescein diacetate (p < 0.05). Conclusions: AE inhibits PS-induced lung inflammation and bacterial colonization in elderly mice, involving IL-10/NF-κB, and redox signaling.

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Section: Discussionsupporting

confidence: 60%

Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice

et al. 2018

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“…Indeed, cancer cachexia patients are exposed to elevated circulating IL-6 levels for weeks, while circulating IL-6 increases punctually after acute exercise. Otherwise, others accompanying our study demonstrated that exercise training inhibits STAT3 phosphorylation-mediated attenuation of proinflammatory condition in chronic diseases (43). Thus, when debating the role of IL-6 and reactive species-dependent STAT3 activation promoted by exercise, we should take in account that downstream target activation and its consequences for skeletal muscle might be different considering health versus disease conditions.…”

Section: Discussionmentioning

confidence: 84%

Resistance Training Attenuates Activation of STAT3 and Muscle Atrophy in Tumor-Bearing Mice

et al. 2022

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PurposeAlthough the role of signal transducers and activators of transcription (STAT3) in cachexia due to the association of circulating IL-6 and muscle wasting has been extensively demonstrated, the effect of resistance training on STAT3 in mediating muscle atrophy in tumor-bearing mice is unknown. The aim of this study is to investigate the effects of resistance exercise training on inflammatory cytokines and oxidative-mediated STAT3 activation and muscle loss prevention in tumor-bearing mice.MethodsMale Swiss mice were inoculated with Ehrlich tumor cells and exposed or not exposed to resistance exercise protocol of ladder climbing. Skeletal muscle STAT3 protein content was measured, compared between groups, and tested for possible association with plasma interleukins and local oxidative stress markers. Components of the ubiquitin-proteasome and autophagy pathways were assessed by real-time PCR or immunoblotting.ResultsResistance training prevented STAT3 excessive activation in skeletal muscle mediated by the overabundance of plasma IL-6 and muscle oxidative stress. These mechanisms contributed to preventing the increased key genes and proteins of ubiquitin-proteasome and autophagy pathways in tumor-bearing mice, such as Atrogin-1, LC3B-II, and Beclin-1. Beyond preventing muscle atrophy, RT also prevented strength loss and impaired locomotor capacity, hallmarks of sarcopenia.ConclusionOur results suggest that STAT3 inhibition is central in resistance exercise protective effects against cancer-induced muscle atrophy and strength loss.

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“… 23 Other groups have also reported the effect of exercise on suppressing COPD and have focused on different mechanisms other than irisin. 63 , 64 NYT may be considered an ergogenic medicine to enhance these favorable effects of exercise.…”

Section: Discussionmentioning

confidence: 99%

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Miyamoto¹,

Asai²,

Kadotani³

et al. 2020

COPD

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Purpose: Sarcopenia, the loss of skeletal muscle mass and strength, is a common systemic consequence of chronic obstructive pulmonary disease (COPD) and is correlated with higher mortality. Ninjin'yoeito (NYT) is a Japanese herbal medicine used to treat athrepsia and anorexia and is reported to ameliorate weight loss and muscular dysfunction. Recent studies have shown that its crude components upregulate the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-related pathway, which is involved in skeletal muscle functions. Here, we examined whether NYT improves skeletal muscle complications by upregulating PGC-1α in COPD model mice. Materials and Methods: Mice were divided into four groups: control, NYT, smoking, and smoking + NYT. The smoking and smoking + NYT groups were exposed to cigarette smoke for 60 min once daily. The mice in the NYT and smoking + NYT groups were fed an NYT-containing diet (3% w/w). We performed cellular analysis of bronchoalveolar lavage fluid, assessed pulmonary morphological changes, examined the expression of PGC-1α mRNA and protein in the gastrocnemius and soleus muscle, measured the hindlimb muscle volume with micro-computed tomography, and determined the myofiber proportion in soleus muscle after 12 weeks. Results: Cigarette smoke exposure resulted in reduced skeletal muscle volume and slowtwitch muscle fibers and development of pulmonary emphysema. NYT feeding induced partial recovery of the damaged alveolar wall; however, NYT did not ameliorate smokeinduced alveolar enlargement. These findings revealed that NYT did not have sufficient efficacy in suppressing pulmonary emphysema. On the other hand, PGC-1α expression in muscle tissue of the NYT-fed mice increased significantly, resulting in suppression of smokeinduced loss of muscle mass and alteration in the muscle fiber distribution. Conclusion: NYT increases PGC-1α expression in the muscle of COPD model mice and is involved in suppressing cigarette smoke-induced muscle complications. NYT may be a novel preventive and therapeutic medication for muscular dysfunctions in COPD.

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

Cited by 13 publications

References 37 publications

Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice

Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice

Resistance Training Attenuates Activation of STAT3 and Muscle Atrophy in Tumor-Bearing Mice

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

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