Inhibition of NADPH Oxidase-Derived Reactive Oxygen Species Decreases Expression of Inflammatory Cytokines in A549 Cells

Wieczfińska, Joanna; Sitarek, Przemysław; Skała, Ewa; Kowalczyk, Tomasz; Pawliczak, Rafał

doi:10.1007/s10753-019-01084-0

Cited by 14 publications

(13 citation statements)

References 85 publications

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“…The AV protective action against UV radiation was due to its stimulating effect on SIRT1 activity (Liu et al, 2020). Moreover, the in vitro activity of AV on PPARγ activity was significantly recognized by Wieczfinska, Sitarek, Skała, Kowalczyk, and Pawliczak (2019), who explore the anti-inflammatory activity of AV is mediated by the activation of PPARγ protein expression. Furthermore, the antioxidant activity of AV was also endorsed by the study conducted by Hassanein, Abd El-Ghafar, et al (2020), who stated that AV has a potential cardioprotective effect through the up-regulation of many antioxidant defense mechanisms, including Nrf2 and cytoglobin.…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective effect of acetovanillone against methotrexate hepatotoxicity: Role of Keap‐1/Nrf2/ARE, IL6/STAT‐3, and NF‐κB/AP‐1 signaling pathways

El-Ghafar

Hassanein

Ali

et al. 2021

Phytotherapy Research

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This study targeted to examine the protective effects of acetovanillone (AV) against methotrexate (MTX)-induced hepatotoxicity. Thirty-two rats were allocated into four groups of eight animals; Group 1: Normal; Group 2: administered AV (100 ml/kg; P.O.) for 10 days; Group 3: challenged with MTX (20 mg/kg, i.p; single dose); Group 4: administered AV 5 days before and 5 days after MTX. For the first time, this study affords evidence for AV's hepatoprotective effects on MTX-induced hepatotoxicity.The underlined mechanisms behind its hepatic protection include counteracting MTX-induced oxidative injury via down-regulation of NADPH oxidase and upregulation of Nrf2/ARE, SIRT1, PPARγ, and cytoglobin signals. Additionally, AV attenuated hepatic inflammation through down-regulation of IL-6/STAT-3 and NF-κB/AP-1 signaling. Network pharmacology analysis exhibited a high enrichment score between the interacting proteins and strongly suggested the intricate and essential role of the target proteins regulating MTX-induced oxidative damage and inflammatory perturbation. Besides, AV increased the in vitro cytotoxic activity of MTX toward PC-3, HeLa, and K562 cancer cell lines. On the whole, our investigation suggested that AV might be regarded as a promising adjuvant for the amelioration of MTX hepatotoxicity and/or increased its in vitro antitumor efficacy, and it could be used in patients receiving MTX.

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Section: Discussionmentioning

confidence: 99%

Hepatoprotective effect of acetovanillone against methotrexate hepatotoxicity: Role of Keap‐1/Nrf2/ARE, IL6/STAT‐3, and NF‐κB/AP‐1 signaling pathways

El-Ghafar

Hassanein

Ali

et al. 2021

Phytotherapy Research

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“…Kim et al reported that APO inhibited the production of proinflammatory cytokines including TNF‐α, IL‐1β, and IL‐6 in experimental asthma mice 18 . Similarly, recent studies have demonstrated that APO decreased TNF‐α and IL‐1β gene expression or downregulation of these cytokines through experimental animal studies or cell cultures on the different inflammatory lung diseases 17,24,45,46 . NOX is an enzyme responsible for ROS production, and proinflammatory stimulus induces intracellular ROS via enzymatic activation of NOX, which ultimately induces activation of NF‐κB 47,48 .…”

Section: Discussionmentioning

confidence: 98%

The protective effects of apocynin in hyperoxic lung injury in neonatal rats

Оздемир

Gökçe

Tekin

et al. 2021

Pediatric Pulmonology

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Aim: Inflammation and oxidate stress are significant factors in the pathogenesis of bronchopulmonary dysplasia (BPD). The aim of this study is to investigate the efficacy of apocynin (APO), an anti-inflammatory, antioxidant, and antiapoptotic drug, in the prophylaxis of neonatal hyperoxic lung injury.Method: This experimental study included 40 neonatal rats divided into the control, APO, BPD, and BPD + APO groups. The control and APO groups were kept in a normal room environment, while the BPD and BPD + APO groups were kept in a hyperoxic environment. The rats in the APO and BPD + APO groups were administered intraperitoneal APO, while the control and BPD rats were administered ordinary saline. At the end of the trial, lung tissue was evaluated with respect to the degree of histopathological injury, apoptosis, oxidant and antioxidant capacity, and severity of inflammation. Result:The BPD and BPD + APO groups exhibited higher mean histopathological injury and alveolar macrophage scores compared to the control and APO groups.Both scores were lower in the BPD + APO group in comparison to the BPD group.The BPD + APO group had a significantly lower average of TUNEL positive cells than the BPD group. The lung tissue examination indicated significantly higher levels of mean malondialdehyde (MDA), total oxidant status (TOS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in the BPD group compared to the control and APO groups. While the TNF-α and IL-1β levels of the BPD + APO group were similar to that of the control group, the MDA and TOS levels were higher compared to the controls and lower compared to the BPD group. The BPD group demonstrated significantly lower levels/activities of mean total antioxidant status, glutathione reductase, superoxide dismutase, glutathione peroxidase in comparison to the control and APO groups. While the mean antioxidant enzyme activity of the BPD + APO group was lower than the control group, it was significantly higher compared to the BPD group. Conclusion:This is the first study in the literature to reveal through an experimental neonatal hyperoxic lung injury that APO, an anti-inflammatory, antioxidant, and antiapoptotic drug, exhibits protective properties against the development of BPD.

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“… Bowen et al (2017a) found that exercise training can reduce the activity of NOX in the diaphragm of mice with COPD, regulate the oxidative stress level, weaken protein degradation, reverse the extrapulmonary damage to the diaphragm caused by smoking, enhance the muscle strength of the diaphragm, and restore the diaphragm function. In addition, the study found that the oxidative stress produced by NOX may be closely related to the expression level of pro-inflammatory factors such as tumor necrosis factor (TNF), and the antioxidant effect was partly responsible for the decrease of the expression level of pro-inflammatory factors ( Wieczfinska et al, 2019 ). Blockage of TNF-α can significantly reduce the number of inflammatory cells and the production of superoxide anion in the diaphragm and improve the structure and function of the diaphragm ( Domínguez-Álvarez et al, 2014 ).…”

Section: Effect and Mechanism Of Exercise On Oxidative Stress Of The Diaphragm In Copdmentioning

confidence: 99%

Effect of Oxidative Stress on Diaphragm Dysfunction and Exercise Intervention in Chronic Obstructive Pulmonary Disease

Zhang

et al. 2021

Front. Physiol.

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Chronic obstructive pulmonary disease (COPD) can cause extrapulmonary injury such as diaphragm dysfunction. Oxidative stress is one of the main factors causing diaphragm dysfunction in COPD. Exercise plays a positive role in the prevention and treatment of diaphragm dysfunction in COPD, and the changes in diaphragm structure and function induced by exercise are closely related to the regulation of oxidative stress. Therefore, on the basis of the review of oxidative stress and the changes in diaphragm structure and function in COPD, this article analyzed the effects of exercise on oxidative stress and diaphragm dysfunction in COPD and explored the possible mechanism by which exercise improves oxidative stress. Studies have found that diaphragm dysfunction in COPD includes the decline of muscle strength, endurance, and activity. Oxidative stress mainly affects the structure and function of the diaphragm in COPD through protein oxidation, protease activation and calcium sensitivity reduction. The effects of exercise on oxidative stress level and diaphragm dysfunction may differ depending on the intensity, duration, and style of exercise. The mechanism of exercise on oxidative stress in the diaphragm of COPD may include improving antioxidant capacity, reducing oxidase activity and improving mitochondrial function.

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Inhibition of NADPH Oxidase-Derived Reactive Oxygen Species Decreases Expression of Inflammatory Cytokines in A549 Cells

Cited by 14 publications

References 85 publications

Hepatoprotective effect of acetovanillone against methotrexate hepatotoxicity: Role of Keap‐1/Nrf2/ARE, IL6/STAT‐3, and NF‐κB/AP‐1 signaling pathways

Hepatoprotective effect of acetovanillone against methotrexate hepatotoxicity: Role of Keap‐1/Nrf2/ARE, IL6/STAT‐3, and NF‐κB/AP‐1 signaling pathways

The protective effects of apocynin in hyperoxic lung injury in neonatal rats

Effect of Oxidative Stress on Diaphragm Dysfunction and Exercise Intervention in Chronic Obstructive Pulmonary Disease

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