N-acetylcysteine decreases lung inflammation and fibrosis by modulating ROS and Nrf2 in mice model exposed to particulate matter

Choi, Seon-Muk; Lee, Pureun‐Haneul; An, Min‐Hyeok; Lee, Yun-Gi; Park, Shinhee; Baek, Ae-Rin; Jang, An‐Soo

doi:10.1080/08923973.2022.2086138

Cited by 4 publications

(13 citation statements)

References 36 publications

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“…NAC was previously found to restore the sensitivity of gefitinib-resistant lung cancer cells to gefitinib that is a major epithelial growth factor receptor tyrosine kinase inhibitor, suggesting the inhibitory effects of NAC on EGFR activation in epithelial cells [24]. With regard to NAC inhibition on mucin hypersecretion caused by RSV infection [25], a previous study, similar as our study, reported that NAC reduce airway inflammation and responsiveness, goblet cell hyperplasia, and lung fibrosis by increasing levels of ROS, nuclear factor erythroid 2-related factor 2, and MUC5AC protein [26]. The present study analyzed the HSPA6 expression in RSV-infected BEAS-2B cells treated with and without NAC.…”

Section: Discussionsupporting

confidence: 78%

N-Acetyl-L-Cysteine Protects Airway Epithelial Cells during Respiratory Syncytial Virus Infection against Mucin Synthesis, Oxidative Stress, and Inflammatory Response and Inhibits HSPA6 Expression

Chi¹,

Shan²,

Cui³

2022

Analytical Cellular Pathology

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Objective. Respiratory syncytial virus (RSV) infection is an important cause of hospitalization of children worldwide, leading to significant morbidity and mortality. RSV infection leads to increasing inflammatory and apoptosis events in the airway epithelium through mechanisms involving ROS generation. The antioxidant N-acetyl-L-cysteine (NAC) has been shown to inhibit influenza virus replication and to reduce the secretion of inflammatory and apoptotic mediators during virus infection. The study aims to investigate the effects of NAC on human bronchial epithelial cells BEAS-2B and HSPA6 expression during RSV infection. Methods. CCK-8 assays were performed to evaluate cell survival. The production of proinflammatory factors, TNF-α, IL-6, IL-1β, IL-18, and MUC5AC was examined by quantitative real-time PCR and ELISA. Oxidative stress was determined by reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH)/glutathione disulfide (GSSG) ratio. Immunoblotting analysis of epidermal growth factor receptor (EGFR) and its phosphorylation was performed. The antiviral effect of NAC was assessed by determining viral titers using plaque assay. Results. RSV infection reduced cell survival, promoted the release of proinflammatory factors, increased the ROS production and MDA concentration, and diminished the SOD activity and GSH/GSSG ratio, all which were attenuated by NAC treatment. Accordingly, NAC treatment inhibited the activation of EGFR and MUC5AC in BEAS-2B cells with RSV infection. Furthermore, NAC administration resulted in a marked decrease in RSV-induced HSPA6 expression in BEAS-2B cells. Concomitantly, EPB treatment led to an evident inhibition of RSV fusion gene and viral replication in RSV-infected BEAS-2B cells. Conclusion. This work supports the use of NAC to exert antimucin synthesis, anti-inflammatory, antioxidant, and antiviral effects on airway epithelium during RSV infection.

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Section: Discussionsupporting

confidence: 78%

N-Acetyl-L-Cysteine Protects Airway Epithelial Cells during Respiratory Syncytial Virus Infection against Mucin Synthesis, Oxidative Stress, and Inflammatory Response and Inhibits HSPA6 Expression

Chi¹,

Shan²,

Cui³

2022

Analytical Cellular Pathology

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“…Furthermore, mast cells generate mainly intracellular ROS following the aggregation of FcεRI, which may act as secondary messenger in the induction of several biological responses. Oxidative stress can activate nuclear factor kappa-B (NF- κ B) pathways to activate gene expression and synthesis of antioxidant enzymes and proinflammatory cytokines, such as IL-6, IL-8, IL-9, and IL-33, which in turn enhances dermal inflammatory infiltrate and histamine release in the affected skin to worsen symptoms [ 55 , 56 ].…”

Section: Development Of Allergic Inflammationmentioning

confidence: 99%

“…In psoriatic skin, reactive species are generated by keratinocytes and activated leukocytes, mostly neutrophils and macrophages, which play a key role in inducing psoriasis-like skin disease [ 54 , 55 , 56 ]. Lactoferrin released by specific neutrophil granules can promote neutrophil-endothelial cell adhesion and, as a source of iron, may promote the Fenton reaction with the generation of the hydroxyl radical (OH•) [ 54 ].…”

Section: Development Of Allergic Inflammationmentioning

confidence: 99%

“…In psoriasis, ROS produced during the inflammatory process affects primarily the polyunsaturated fatty acid in a biological system, forming a lipid peroxidation product MDA, which serves as an important biological marker of lipid peroxidation. The increased levels of other reactive species, such as nitric oxide (NO), superoxide anion (O 2 •−) and hydrogen peroxide (H 2 O 2 ) have been found in the skin of psoriatic patients [ 54 , 55 , 56 ]. Hydrogen peroxide (H 2 O 2 ) and the superoxide anion (O 2 •−) can be generated by the action of the enzyme xanthine oxidase, which displays a higher activity in psoriatic epidermis [ 54 , 55 , 56 ].…”

Section: Development Of Allergic Inflammationmentioning

confidence: 99%

“…The increased levels of other reactive species, such as nitric oxide (NO), superoxide anion (O 2 •−) and hydrogen peroxide (H 2 O 2 ) have been found in the skin of psoriatic patients [ 54 , 55 , 56 ]. Hydrogen peroxide (H 2 O 2 ) and the superoxide anion (O 2 •−) can be generated by the action of the enzyme xanthine oxidase, which displays a higher activity in psoriatic epidermis [ 54 , 55 , 56 ]. Additionally, cytokines such as tumor necrosis factor alpha can contribute to H 2 O 2 production [ 54 ].…”

Section: Development Of Allergic Inflammationmentioning

confidence: 99%

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Allergic Inflammation: Effect of Propolis and Its Flavonoids

Oršolić

2022

Molecules

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The incidence of allergic diseases and their complications are increasing worldwide. Today, people increasingly use natural products, which has been termed a “return to nature”. Natural products with healing properties, especially those obtained from plants and bees, have been used in the prevention and treatment of numerous chronic diseases, including allergy and/or inflammation. Propolis is a multi-component resin rich in flavonoids, collected and transformed by honeybees from buds and plant wounds for the construction and adaptation of their nests. This article describes the current views regarding the possible mechanisms and multiple benefits of flavonoids in combating allergy and allergy-related complications. These benefits arise from flavonoid anti-allergic, anti-inflammatory, antioxidative, and wound healing activities and their effects on microbe-immune system interactions in developing host responses to different allergens. Finally, this article presents various aspects of allergy pathobiology and possible molecular approaches in their treatment. Possible mechanisms regarding the antiallergic action of propolis on the microbiota of the digestive and respiratory tracts and skin diseases as a method to selectively remove allergenic molecules by the process of bacterial biotransformation are also reported.

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PRDX1 negatively regulates bleomycin-induced pulmonary fibrosis via inhibiting the epithelial-mesenchymal transition and lung fibroblast proliferation in vitro and in vivo

et al. 2023

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Background Pulmonary fibrosis is a major category of end-stage changes in lung diseases, characterized by lung epithelial cell damage, proliferation of fibroblasts, and accumulation of extracellular matrix. Peroxiredoxin 1 (PRDX1), a member of the peroxiredoxin protein family, participates in the regulation of the levels of reactive oxygen species in cells and various other physiological activities, as well as the occurrence and development of diseases by functioning as a chaperonin. Methods Experimental methods including MTT assay, morphological observation of fibrosis, wound healing assay, fluorescence microscopy, flow cytometry, ELISA, western blot, transcriptome sequencing, and histopathological analysis were used in this study. Results PRDX1 knockdown increased ROS levels in lung epithelial cells and promoted epithelial-mesenchymal transition (EMT) through the PI3K/Akt and JNK/Smad signalling pathways. PRDX1 knockout significantly increased TGF-β secretion, ROS production, and cell migration in primary lung fibroblasts. PRDX1 deficiency also increased cell proliferation, cell cycle circulation, and fibrosis progression through the PI3K/Akt and JNK/Smad signalling pathways. BLM treatment induced more severe pulmonary fibrosis in PRDX1-knockout mice, mainly through the PI3K/Akt and JNK/Smad signalling pathways. Conclusions Our findings strongly suggest that PRDX1 is a key molecule in BLM-induced lung fibrosis progression and acts through modulating EMT and lung fibroblast proliferation; therefore, it may be a therapeutic target for the treatment of BLM-induced lung fibrosis.

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N-acetylcysteine decreases lung inflammation and fibrosis by modulating ROS and Nrf2 in mice model exposed to particulate matter

Cited by 4 publications

References 36 publications

N-Acetyl-L-Cysteine Protects Airway Epithelial Cells during Respiratory Syncytial Virus Infection against Mucin Synthesis, Oxidative Stress, and Inflammatory Response and Inhibits HSPA6 Expression

N-Acetyl-L-Cysteine Protects Airway Epithelial Cells during Respiratory Syncytial Virus Infection against Mucin Synthesis, Oxidative Stress, and Inflammatory Response and Inhibits HSPA6 Expression

Allergic Inflammation: Effect of Propolis and Its Flavonoids

PRDX1 negatively regulates bleomycin-induced pulmonary fibrosis via inhibiting the epithelial-mesenchymal transition and lung fibroblast proliferation in vitro and in vivo

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