Role of oxidative stress in the pathogenesis of COPD

Nucera, Francesco; Mumby, Sharon; Paudel, Keshav Raj; Dharwal, Vivek; Stefano, Antonino Di; Casolaro, Vincenzo; Hansbro, Philip M.; Adcock, Ian M.; Caramori, Gaetano

doi:10.23736/s0026-4806.22.07972-1

Cited by 43 publications

(19 citation statements)

References 168 publications

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“…Likewise, these cells are a source of reactive oxygen and nitrogen species (ROS and RNS); the increased production of ROS/RNS affects phagocytosis and activates NF-κB and p38 MAPK, which enhance the expression of pro-inflammatory genes [69]. Oxidative stress plays a crucial role in the pathogenesis of COPD; the imbalance between the production of oxidants and antioxidant defenses may also contribute to the worsening of the disease during acute exacerbation [70]. Studies have measured hydrogen peroxide (H 2 O 2 ) in the exhaled air condensate.…”

Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

Sierra-Vargas

Montero-Vargas

Debray-García

et al. 2023

IJMS

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Redox regulation participates in the control of various aspects of metabolism. Reactive oxygen and nitrogen species participate in many reactions under physiological conditions. When these species overcome the antioxidant defense system, a distressed status emerges, increasing biomolecular damage and leading to functional alterations. Air pollution is one of the exogenous sources of reactive oxygen and nitrogen species. Ambient airborne particulate matter (PM) is important because of its complex composition, which includes transition metals and organic compounds. Once in contact with the lungs’ epithelium, PM components initiate the synthesis of inflammatory mediators, macrophage activation, modulation of gene expression, and the activation of transcription factors, which are all related to the physiopathology of chronic respiratory diseases, including cancer. Even though the pathophysiological pathways that give rise to the development of distress and biological damage are not fully understood, scientific evidence indicates that redox-dependent signaling pathways are involved. This article presents an overview of the redox interaction of air pollution inside the human body and the courses related to chronic respiratory diseases.

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Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

Sierra-Vargas

Montero-Vargas

Debray-García

et al. 2023

IJMS

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“…Another fundamental driving factor of COPD is oxidative stress, which is caused by an imbalance between the production and elimination, through antioxidant detoxification mechanisms, of reactive oxygen species (ROS) [ 7 , 34 , 35 ]. A fundamental mediator of cellular detoxification is glutathione [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

Agarwood Oil Nanoemulsion Attenuates Cigarette Smoke-Induced Inflammation and Oxidative Stress Markers in BCi-NS1.1 Airway Epithelial Cells

et al. 2023

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Chronic obstructive pulmonary disease (COPD) is an irreversible inflammatory respiratory disease characterized by frequent exacerbations and symptoms such as cough and wheezing that lead to irreversible airway damage and hyperresponsiveness. The primary risk factor for COPD is chronic cigarette smoke exposure, which promotes oxidative stress and a general pro-inflammatory condition by stimulating pro-oxidant and pro-inflammatory pathways and, simultaneously, inactivating anti-inflammatory and antioxidant detoxification pathways. These events cause progressive damage resulting in impaired cell function and disease progression. Treatments available for COPD are generally aimed at reducing the symptoms of exacerbation. Failure to regulate oxidative stress and inflammation results in lung damage. In the quest for innovative treatment strategies, phytochemicals, and complex plant extracts such as agarwood essential oil are promising sources of molecules with antioxidant and anti-inflammatory activity. However, their clinical use is limited by issues such as low solubility and poor pharmacokinetic properties. These can be overcome by encapsulating the therapeutic molecules using advanced drug delivery systems such as polymeric nanosystems and nanoemulsions. In this study, agarwood oil nanoemulsion (agarwood-NE) was formulated and tested for its antioxidant and anti-inflammatory potential in cigarette smoke extract (CSE)-treated BCi-NS1.1 airway basal epithelial cells. The findings suggest successful counteractivity of agarwood-NE against CSE-mediated pro-inflammatory effects by reducing the expression of the pro-inflammatory cytokines IL-1α, IL-1β, IL-8, and GDF-15. In addition, agarwood-NE induced the expression of the anti-inflammatory mediators IL-10, IL-18BP, TFF3, GH, VDBP, relaxin-2, IFN-γ, and PDGF. Furthermore, agarwood-NE also induced the expression of antioxidant genes such as GCLC and GSTP1, simultaneously activating the PI3K pro-survival signalling pathway. This study provides proof of the dual anti-inflammatory and antioxidant activity of agarwood-NE, highlighting its enormous potential for COPD treatment.

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“…From 1980 to 2017, COPD was the third leading cause of death in the world, and the mortality rate will continue to increase in the next 20 years [1]. Chronic and long-period inhalation of cigarette smoke (CS) is considered a major cause of COPD [2]. CS can alter airway epithelial barrier function, increase oxidative stress, promote airway epithelial aging and activate proinflammatory pathways [3].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Ginkgo biloba Extract on Autophagy in Human Macrophages Stimulated by Cigarette Smoke Extract

Zhang¹,

Zhu²,

Zhang³

et al. 2023

Front. Biosci. (Landmark Ed)

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Objective: To investigate the effects of Ginkgo biloba extract (GBE) on autophagy in human macrophages stimulated by cigarette smoke extract (CSE). Methods: The human monocyte cell line U937 was cultured in vitro, and phorbol ester (PMA) was added to the cell culture medium to induce differentiation into human macrophages. CSE was prepared by traditional methods for experiments. The cells were divided into four groups: the blank group, the CSE model group, the GBE + CSE group, and the rapamycin + CSE group. Immunofluorescence was used to identify human macrophages, transmission electron microscopy was used to observe the ultrastructure of human macrophages in each group, ELISA was used to measure the amount of IL-6 and IL-10 in the supernatant from each group of cells, the mRNA levels of p62, ATG5, ATG7, and Rab7 were measured by real-time qPCR, and the protein expression levels of p62, ATG5, ATG7, and Rab7 were measured by Western blotting. Results: U937 cells were successfully differentiated into human macrophages after induction with PMA. The CSE model group had many more autophagosomes than the blank group. Compared with the CSE model group, the GBE + CSE group and the rapamycin + CSE group had significantly more autophagolysosomal. Compared with the other groups, the CSE model group had a higher level of IL-6 but a lower level of IL-10 in the supernatant (p < 0.05). Compared with the blank group, the mRNA and protein expression levels of p62 in the CSE model group were significantly decreased, while the mRNA and protein expression levels of ATG5 and ATG7 were significantly increased in the CSE model group (p < 0.05). No difference was found in the mRNA and protein expression levels of Rab7 between the blank group and the CSE model group. Compared with the CSE model group, the IL-6 level in the GBE + CSE group and the rapamycin + CSE group cell culture supernatant decreased significantly, p62 mRNA and protein expression significantly decreased, while ATG5, ATG7, and Rab7 mRNA and protein expression levels were significantly increased (p < 0.05). Moreover, increased LC3-II/LC3-I ratio were also found in the GBE + CSE group and the rapamycin + CSE group compared with the CSE model group. Conclusions: GBE could promote the fusion of autophagosomes and lysosomes in human macrophages, enhance the autophagy function of human macrophages, and reduce the damaging effect of CSE on the autophagy function of macrophages.

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Role of oxidative stress in the pathogenesis of COPD

Cited by 43 publications

References 168 publications

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

Agarwood Oil Nanoemulsion Attenuates Cigarette Smoke-Induced Inflammation and Oxidative Stress Markers in BCi-NS1.1 Airway Epithelial Cells

The Effects of Ginkgo biloba Extract on Autophagy in Human Macrophages Stimulated by Cigarette Smoke Extract

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