Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type II alveolar epithelial cells

Cheng, Zhiqiang; Han, Jiaguang; Sun, Peng; Weng, Yu-ying; Chen, Jiao; Wu, Guo-yan; Ma, Hongxia

doi:10.5847/wjem.j.issn.1920-8642.2012.01.010

Cited by 11 publications

(5 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Secondly, as it has been clinically used for many years, its safety has been well proven. Thirdly, many studies have demonstrated the effects of edaravone against lung injuries, such as hepatic ischemia-reperfusion-induced lung injury, black gunpowder smog-induced lung injury induced, lipopolysaccharide-induced acute lung injury, paraquat-induced lung injury [47][48][49][50]. Taken together, these results indicate the potential benefit of edaravone in various lung injuries due to oxidative stress besides hyperoxia.…”

Section: Discussionmentioning

confidence: 71%

Edaravone protects rats and human pulmonary alveolar epithelial cells against hyperoxia injury: heme oxygenase-1 and PI3K/Akt pathway may be involved

Cao

Feng

Ning

et al. 2015

Experimental Lung Research

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 71%

Edaravone protects rats and human pulmonary alveolar epithelial cells against hyperoxia injury: heme oxygenase-1 and PI3K/Akt pathway may be involved

Cao

Feng

Ning

et al. 2015

Experimental Lung Research

View full text Add to dashboard Cite

show abstract

“…Herbicide paraquat toxicity can cause severe oxidative injury in the lungs (24). In A549 cells treated with paraquat, administration of Eda decreased the levels of intracellular ROS and malondialdehyde (MDA) but increased the levels of superoxide dismutase (SOD) (25). In a canine lung transplantation model, Eda significantly decreased lung wet/dry ratios, MDA levels and myeloperoxidase activity (26).…”

Section: Edaravone Attenuates Experimental Asthma In Mice Through Indmentioning

confidence: 99%

Edaravone attenuates experimental asthma in mice through induction of HO‑1 and the Keap1/Nrf2 pathway

Pan

Feng

et al. 2019

Exp Ther Med

View full text Add to dashboard Cite

Asthma is a chronic disease that threatens public health worldwide. Multiple studies have shown that oxidative stress plays an important role in the pathogenesis of asthma. Edaravone (Eda), a free radical scavenger, has been found to have a protective effect against lung injury due to its ability to eliminate reactive oxygen species. The present study aimed to investigate the effect of Eda on asthma and the mechanism underlying its actions. An experimental asthma model was induced in mice, before they were treated with different doses of Eda. Measurements of airway responsiveness to methacholine (Mch), cell counts and cytokine levels in bronchoalveolar lavage fluid (BALF) and of the oxidative products and antioxidant enzymes in lung tissue were taken in these asthma model mice and compared with control mice. Protein levels of kelch-like ECH-associated protein-1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) were determined in the lung tissue of normal mice and Nrf2 and HO-1-deficient mice subject to the asthma model to investigate the mechanisms underlying Eda action. The results indicated that Eda effectively reduced airway responsiveness to Mch. The total number of cells and the numbers of eosinophils, lymphocytes and neutrophils in BALF of asthma model mice were also significantly reduced by Eda treatment when compared with normal saline treatment. Eda treatment significantly alleviated perivascular edema, peribronchial inflammation and macrophage infiltration in the alveolar space and decreased the levels of inflammatory cytokines released in BALF compared with control. Eda also significantly reduced the levels of oxidative stress markers in BALF and restored the levels of antioxidative enzyme, superoxide dismutase, when compared with control. The Keap1/Nrf2 ratio was significantly decreased with Eda compared with control due to an increase in Nrf2 and a decrease in Keap1 expression. HO-1 expression was increased by Eda. The airway responsiveness of Nrf2-/mice or HO-1-/mice to Mch was significantly higher compared with normal mice treated with Eda. Taken together, the results of the present study show that Eda exerts anti-inflammatory and antioxidative effects, which suggests a potential use for Eda in reduction of asthma severity. The activated Keap1/Nrf2 pathway and HO-1 may be involved in the anti-asthmatic effect of Eda.

show abstract

“…ATII is one of the important cell populations on the alveolar surface, which secretes and synthesizes active substances on the lung surface, helps promote the transmembrane transport of fluid and electrolytes on the alveolar surface, supplements and differentiates ATI and plays an important role in detoxicating and metabolizing poisons and drugs. The apoptosis of ATII is involved in the entire process of acute lung injury [ 16 ]. In this study, the ATII HR injury model was established through 24-h hypoxia and 4-h reoxygenation to simulate IRI of the lungs.…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV attenuates hypoxia/reoxygenation injury-induced apoptosis of type II alveolar epithelial cells through miR-21-5p

Yao

Shi

et al. 2021

Bioengineered

View full text Add to dashboard Cite

We aimed to explore the role of miR-21-5p in the inhibitory effects of astragaloside IV (As-IV) on hypoxia/reoxygenation injury-induced apoptosis of type II alveolar epithelial cells. Rat type II alveolar epithelial cells RLE-6TN were cultured in vitro and randomly divided into control (C), hypoxia/reoxygenation injury (H/R), As-IV and miR-21-5p-siRNA + As-IV groups (n = 6). H/R model was established by 24 h of hypoxia and 4 h of reoxygenation. As-IV group was given 1 nmol/L As-IV and incubated for 1 h before modeling. MiR-21-5p-siRNA + As-IV group was transfected with 50 nmol/L miR-21-5p-siRNA. After 48 h, they were incubated with 1 nmol/L As-IV for 1 h before modeling. Cell viability was detected by cell counting kit-8 assay, and apoptosis rate was detected by flow cytometry. The expression levels of TLR4 and NF-κB were measured by immunofluorescence assay. The targeting relationship between miR-21-5p and TLR4 was determined by luciferase assay. Compared with H/R group, the cell viability, miR-21-5p, bax and cleaved caspase-3 expressions of As-IV group increased, apoptosis rate and Bcl-2 expression decreased, and TLR4 and NF-κB expressions were down-regulated (P < 0.05). Compared with As-IV group, the cell viability, miR-21-5p, bax and cleaved caspase-3 expressions of miR-21-5p-siRNA + As-IV group decreased, apoptosis rate and Bcl-2 expression increased, and the expressions of TLR4 and NF-κB were up-regulated (P < 0.05). As-IV up-regulates miR-21-5p expression, inhibits the TLR4/NF-κB signaling pathway and suppresses the apoptosis of type II alveolar epithelial cells during hypoxia/ reoxygenation injury.

show abstract

Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type II alveolar epithelial cells

Cited by 11 publications

References 22 publications

Edaravone protects rats and human pulmonary alveolar epithelial cells against hyperoxia injury: heme oxygenase-1 and PI3K/Akt pathway may be involved

Edaravone protects rats and human pulmonary alveolar epithelial cells against hyperoxia injury: heme oxygenase-1 and PI3K/Akt pathway may be involved

Edaravone attenuates experimental asthma in mice through induction of HO‑1 and the Keap1/Nrf2 pathway

Astragaloside IV attenuates hypoxia/reoxygenation injury-induced apoptosis of type II alveolar epithelial cells through miR-21-5p

Contact Info

Product

Resources

About