New Insights into the Nrf-2/HO-1 Signaling Axis and Its Application in Pediatric Respiratory Diseases

Zhang, Xueyan; Ding, Mingchao; Zhu, Ping; Huang, Huanlei; Zhuang, Quan; Shen, Jie; Cai, Yi; Zhao, Mingyi; He, Qing

doi:10.1155/2019/3214196

Cited by 61 publications

(39 citation statements)

References 69 publications

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“…The Nrf-2/HO-1 pathway is involved in many functions including mitochondrial oxidative stress, autophagy, and programmed cell death [24]. Nrf-2, when translocated into the nucleus, stimulates transcription of genes that encode detoxifying and antioxidant enzymes, contributing to cellular protection by reducing oxidative stress [25].…”

Section: Roles Of Nuclear Factor Erythroid 2-related Factor 2/heme Oxmentioning

confidence: 99%

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.

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Section: Roles Of Nuclear Factor Erythroid 2-related Factor 2/heme Oxmentioning

confidence: 99%

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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“… 24 Nrf2 was a transcription factor that binds to the promoter of the HO-1 gene leading to anti-inflammation and anti-oxidation responses. 25 Dysiarenone significantly promoted the expression of Nrf2 and HO-1 protein in macrophages at a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 93%

Dysiarenone from Marine Sponge Dysidea arenaria Attenuates ROS and Inflammation via Inhibition of 5-LOX/NF-κB/MAPKs and Upregulation of Nrf-2/OH-1 in RAW 264.7 Macrophages

Hu¹,

Zhang²,

Chen³

et al. 2021

JIR

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Background Marine natural products harbor a variety of pharmacological activities, and the sea species have been becoming a main source of new drug candidate. In pursuit of safer and more effective anti-inflammation drug, the anti-inflammatory activities, anti-oxygenation effects and underlying molecular mechanisms of compound dysiarenone from Dysidea arenaria were investigated via LPS-induced RAW 264.7 cell model. Methods Firstly, RAW 264.7 cells have been stimulated with LPS and treated with dysiarenone, and the cell viability of the LPS-treated RAW 264.7 cells was examined. One-step method, DCFH-DA fluorescence probe method was used to detect reactive oxygen species (ROS). The modulation of dysiarenone on anti-inflammation was detected by enzyme-linked immunosorbent assay by measuring the release of inflammatory cytokines (TNF-α and IL-6), and inflammatory mediators (LTB4). Further, the underlying anti-inflammatory mechanism of dysiarenone was explored by determining the expression of inducible 5-LOX, MAPKs, p-Akt, and p-NF-κB p65. Oxidative stress is tightly connected with inflammation, which was also evaluated through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (OH-1) signaling pathway. Results Our study unraveled that dysiarenone between 2 and 8 µM reduces the inflammation responses via suppressing the production of inflammatory cytokines (TNF-α and IL-6) and inflammatory mediators (LTB 4 ). Dysiarenone down-regulated the protein levels of inducible 5-LOX via the inhibition of phosphorylation of MAPKs (including p38, ERK), Akt and NF-κB p65. Additionally, dysiarenone decreases ROS accumulation by upregulating HO-1 expression via nuclear translocation of Nrf2. Conclusion In conclusion, we demonstrated that dysiarenone possesses anti-inflammation and anti-oxidation activity via inhibiting 5-LOX/NF-κB/MAPK and Nrf2/HO-1 signaling pathway. Dysiarenone might be a promising lead compound for inflammatory diseases.

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“…In the case of InCl 3 -exposed cells, the possibility that indium ions interact with proteins contained in FBS to form aggregates, which partially contribute to the genotoxicity, may not be neglected, but their contribution appears to be small under the conditions used. A549 cells have constitutively active Nrf-2 32 , which contributes to their protection against oxidative stress injury 33 . In this study, indium compounds caused clear nitrative DNA lesions in A549 cells, suggesting that indium-induced oxidative and nitrative stress overwhelmed their antioxidative potential.…”

Section: Discussionmentioning

confidence: 99%

Nitrative DNA damage in lung epithelial cells exposed to indium nanoparticles and indium ions

Sharif

Kobayashi

Afroz

et al. 2020

Sci Rep

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indium compounds have been widely used in manufacturing displays of mobile phones, computers and televisions. However, inhalation exposure to indium compounds causes interstitial pneumonia in exposed workers and lung cancer in experimental animals. 8-Nitroguanine (8-nitroG) is a mutagenic DNA lesion formed under inflammatory conditions and may participate in indium-induced carcinogenesis. In this study, we examined 8-nitroG formation in A549 cultured human lung epithelial cells treated with indium compounds, including nanoparticles of indium oxide (In 2 o 3) and indium-tin oxide (ITO), and indium chloride (InCl 3). We performed fluorescent immunocytochemistry to examine 8-nitroG formation in indium-exposed A549 cells. All indium compounds significantly increased 8-nitroG formation in A549 cells at 5 ng/ml after 4 h incubation. 8-NitroG formation was largely reduced by 1400 W, methyl-β-cyclodextrin (MBCD) and monodansylcadaverine (MDC), suggesting the involvement of nitric oxide synthase and endocytosis. 8-NitroG formation in A549 cells was also largely suppressed by small interfering RNA (siRNA) for high-mobility group box-1 (HMGB1), receptor for advanced glycation and end products (AGER, RAGE) and Toll-like receptor 9 (TLR9). These results suggest that indium compounds induce inflammation-mediated DNA damage in lung epithelial cells via the HMGB1-RAGE-TLR9 pathway. This mechanism may contribute to indium-induced genotoxicity in the respiratory system.

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New Insights into the Nrf-2/HO-1 Signaling Axis and Its Application in Pediatric Respiratory Diseases

Cited by 61 publications

References 69 publications

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Dysiarenone from Marine Sponge Dysidea arenaria Attenuates ROS and Inflammation via Inhibition of 5-LOX/NF-κB/MAPKs and Upregulation of Nrf-2/OH-1 in RAW 264.7 Macrophages

Nitrative DNA damage in lung epithelial cells exposed to indium nanoparticles and indium ions

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