<i>In vivo</i>and<i>in vitro</i>evidence for the involvement of Nrf2-antioxidant response element signaling pathway in the inflammation and oxidative stress induced by particulate matter (PM10): the effective role of gallic acid

Radan, Maryam; Dianat, Mahin; Badavi, Mohammad; Mard, Seyyed Ali; Bayati, Vahid

doi:10.1080/10715762.2018.1563689

Cited by 53 publications

(34 citation statements)

References 40 publications

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“…Nrf2 24 is a major contributor to cellular defense against oxidative damage. There was a significant decrease in the expression of Nrf2 and its upstream regulator genes upon PM 10 exposure, suggesting that Nrf2 is involved in PM 10induced oxidative damage 24 .…”

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Mechanisms of ultrafine particle-induced respiratory health effects

2020

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Particulate matter (PM) is the principal component of air pollution. PM includes a range of particle sizes, such as coarse, fine, and ultrafine particles. Particles that are <100 nm in diameter are defined as ultrafine particles (UFPs). UFPs are found to a large extent in urban air as both singlet and aggregated particles. UFPs are classified into two major categories based on their source. Typically, UFPs are incidentally generated in the environment, often as byproducts of fossil fuel combustion, condensation of semivolatile substances or industrial emissions, whereas nanoparticles are manufactured through controlled engineering processes. The primary exposure mechanism of PM is inhalation. Inhalation of PM exacerbates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain unclear. This review offers insights into the mechanisms by which particles, including UFPs, influence airway inflammation and discusses several mechanisms that may explain the relationship between particulate air pollutants and human health, particularly respiratory health. Understanding the mechanisms of PMmediated lung injury will enhance efforts to protect at-risk individuals from the harmful health effects of air pollutants.

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Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Mechanisms of ultrafine particle-induced respiratory health effects

2020

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“…PAHs and their derivatives are especially important because they are able to generate ROS in tissues 19 .Genes encoding key antioxidant enzymes are important for maintaining intracellular redox homeostasis through the antioxidant response element (ARE) found within the promoter regions of these genes 20 . The transcription factor nuclear factor erythroid-derived 2-like 2 (NFE2L2, also known as Nrf2) induces ARE genes as part of a protective response against oxidative challenge to organelles and macromolecules 21 .Recent in vivo and in vitro models have shown that the oxidative damage caused by PM exposure can activate the Nrf2-antioxidant response element signalling pathway 22,23 . Additionally, A549 cell and murine alveolar macrophage cultures exposed to DEP have shown increased Nrf2 and HO-1 (an Nrf2 target gene) expression levels 24 .There is evidence that some autophagy genes, such as Atg5, Atg4D and SQSTM1/p62, have ARE promoter regions, and these promotors may be regulated through Nrf2 activity 25 .…”

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confidence: 99%

“…Recent in vivo and in vitro models have shown that the oxidative damage caused by PM exposure can activate the Nrf2-antioxidant response element signalling pathway 22,23 . Additionally, A549 cell and murine alveolar macrophage cultures exposed to DEP have shown increased Nrf2 and HO-1 (an Nrf2 target gene) expression levels 24 .…”

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confidence: 99%

Nrf2 positively regulates autophagy antioxidant response in human bronchial epithelial cells exposed to diesel exhaust particles

Frias

Gomes

Yoshizaki

et al. 2020

Sci Rep

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Diesel exhaust particles (DEP) are known to generate reactive oxygen species in the respiratory system, triggering cells to activate antioxidant defence mechanisms, such as Keap1-Nrf2 signalling and autophagy. The aim of this study was to investigate the relationship between the Keap1-Nrf2 signalling and autophagy pathways after DEP exposure. BEAS-2B cells were transfected with silencing RNA (siRNA) specific to Nrf2 and exposed to DEP. The relative levels of mRNA for Nrf2, NQO1, HO-1, LC3B, p62 and Atg5 were determined using RT-PCR, while the levels of LCB3, Nrf2, and p62 protein were determined using Western blotting. The autophagy inhibitor bafilomycin caused a significant decrease in the production of Nrf2, HO-1 and NQO1 compared to DEPs treatment, whereas the Nrf2 activator sulforaphane increased the LC3B (p = 0.020) levels. BEAS-2B cells exposed to DEP at a concentration of 50 μg/mL for 2 h showed a significant increase in the expression of LC3B (p = 0.001), p62 (p = 0.008), Nrf2 (p = 0.003), HO-1 (p = 0.001) and NQO1 (p = 0.015) genes compared to control. In siRNAtransfected cells, the LC3B (p < 0.001), p62 (p = 0.001) and Atg5 (p = 0.024) mRNA levels and the p62 and LC3II protein levels were decreased, indicating that Nrf2 modulated the expression of autophagy markers (R < 1). These results imply that, in bronchial cells exposed to DEP, the Nrf2 system positively regulates autophagy to maintain cellular homeostasis.Chronic exposure to air pollution has been associated with adverse effects on the health of individuals 1 , such as inflammation 2-4 and mucociliary clearance dysfunction 5 of the respiratory system. Air pollution particulate matter (PM) induces oxidative stress in airway tissues, causing living organisms to activate their defences to prevent cell death 6-8 . One mechanism that cells use for defence against oxidative stress is autophagy, which is a homeostatic process that reduces cytoplasmic volume by degrading damaged organelles and proteins through a lysosome-dependent degradation process, and new organelles and proteins are synthesized as replacements 9-11 . Previous studies have emphasized that exposure to PM induces the generation of reactive oxygen species (ROS) and increases the levels of autophagy and cell death [12][13][14] . Some of the most harmful components of urban PM are derived from diesel exhaust particles (DEP) 15,16 . Usually, composed of carbon nuclei, DEP have large surface areas that can adsorb other chemicals in the www.nature.com/scientificreports www.nature.com/scientificreports/ environment, such as polycyclic aromatic hydrocarbons (PAHs), sulphate, nitrate, metals, carbon monoxide, aldehydes and various low molecular weight hydrocarbons 17,18 . PAHs and their derivatives are especially important because they are able to generate ROS in tissues 19 .Genes encoding key antioxidant enzymes are important for maintaining intracellular redox homeostasis through the antioxidant response element (ARE) found within the promoter regions of these genes 20 . The transcription fact...

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“…Fine and ultra ne PMs have been reported to induce lung diseases through generation of ROS and oxidative stress as well as activation of innate and adaptive immunity, leading to cell barrier and tissue damage (22,23). Several known promoters of in ammatory response, such as nuclear factor-κB (NF-κB), activation protein-1 (AP-1), nuclear factor erythroid 2 related factor 2 (Nrf2), and CREB-binding proteins (CBPs), are activated by oxidative stress (24)(25)(26). In our study, we observed signi cantly higher levels of oxidative stress and IL-6 in together with up-regulation of in ammation-related pathways including acute phase response and complement system in rats exposed to PM 1 for 3 months.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

Jheng¹,

Putri²,

Chuang³

et al. 2020

Preprint

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Background: Exposure to particulate matter (PM) pollution has direct impacts on the respiratory organs, yet the molecular alterations underlying PM-induced pulmonary injury remain unclear. In this study, we investigated the effect of PM on lung tissues of SD rats with whole-body exposure to traffic-related PM1 (< 1 mm in aerodynamic diameter) pollutants and compared it with rats exposed to high-efficiency particulate air-filtered gaseous pollutants and clean air control for 3 and 6 months. Lung function and histological examinations as well as quantitative proteomics analysis and functional validation were performed. Results: The rats in 6-month PM1-exposed group showed significant decline in lung function by decreased forced expiratory flow and forced expiratory volume, but the histological analysis revealed an earlier lung damage evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2,673 proteins which highlighted dysregulations on proteins involved in oxidative stress, cellular metabolisms, calcium signaling, inflammatory responses, and actin dynamics. The presence of fine particles specifically enhanced the oxidative stress and inflammatory reactions under sub-chronic exposure of traffic-related PM1 and suppressed the glucose metabolism and actin cytoskeleton signaling which might lead to repair failure and thus lung function decline after chronic exposure of traffic-related PM1. A detailed pathogenic mechanism was proposed to depict the temporal and dynamic molecular regulations associated with PM1-induced lung injury.Conclusion: Our study explored the earlier lung injury prior to lung function decline and proposed potential molecular features for traffic-related PM1-induced lung injury.

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In vivoandin vitroevidence for the involvement of Nrf2-antioxidant response element signaling pathway in the inflammation and oxidative stress induced by particulate matter (PM10): the effective role of gallic acid

Cited by 53 publications

References 40 publications

Mechanisms of ultrafine particle-induced respiratory health effects

Mechanisms of ultrafine particle-induced respiratory health effects

Nrf2 positively regulates autophagy antioxidant response in human bronchial epithelial cells exposed to diesel exhaust particles

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

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