Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability

Ma, Xiaohong; Liu, Xiangyong; Feng, Jiali; Zhang, Dong; Huang, Lanqing; Li, Dongxiao; Yin, Liang; Li, Lan; Wang, Xiaozhi

doi:10.1007/s10753-019-01052-8

Cited by 27 publications

(23 citation statements)

References 35 publications

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“…ARDS is a severe inflammatory disorder of the lung and is associated with oxidative damage. 11,12 Recently, Thompson et al summarized the current understanding of ARDS, including the detailed role of inflammation in the pathogenesis of ARDS. 10 Lung injury in patients with ARDS begins with damage to alveolar endothelial cells and epithelial cells, as well as the creation of fluid accumulation in the lung.…”

Section: Discussionmentioning

confidence: 99%

“…8 Ma et al reported that fraxin attenuates LPS-induced ARDS by inhibiting inflammatory responses and reducing oxidative stress while reducing fluid leakage by reducing pulmonary vascular permeability. 12 These reflect the vital role of oxidative stress in ARDS.…”

Section: Discussionmentioning

confidence: 99%

“…Research has shown that ARDS is a severe inflammatory disorder of the lungs and is associated with oxidative damage. [8][9][10][11][12] At the same time, red blood cell distribution width (RDW) reflects the degree of inflammation and oxidative stress to some extent. [13][14][15][16] For the most part, RDW determined by the width of the distribution curve of the corpuscular volume is an indicator of an anaemia diagnosis.…”

Section: Introductionmentioning

confidence: 99%

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Red blood cell distribution width is associated with mortality risk in patients with acute respiratory distress syndrome based on the Berlin definition: A propensity score matched cohort study

Chen

et al. 2020

Heart & Lung

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Background: Acute respiratory distress syndrome (ARDS) is a severe inflammatory disorder of the lungs and is associated with oxidative damage. However, red blood cell distribution width (RDW), as an indicator of body response to inflammation and oxidative stress, has not been studied for its relationship with ARDS as diagnosed by the Berlin definition. Objectives: To examine the value of RDW in predicting the prognosis of in patients with ARDS. Methods: This is a retrospective study based on the Medical Information Mart for Intensive Care III (MIMIC-III) database. Berlin-defined ARDS patients using mechanical ventilation for more than 48 hours were selected using structured query language. The primary statistical methods were propensity score matching and sensitivity analysis, including an inverse probability weighting model to ensure the robustness of our findings. Results: A total of 529 intensive care unit (ICU) patients with ARDS according to the Berlin definition were enrolled in the study. The adjusted OR showed an adverse effect between the higher RDW group and 30-day mortality [OR 2.33, 95% CI (1.15À4.75), P=0.019]. However, we found that length of ICU stay was not related to RDW (P=0.167), and in the anaemia group, RDW was poorly predictive of 30-day mortality (P=0.307). Conclusion:In unselected ARDS patients, higher RDW was associated with higher 30-day mortality rate. Further investigation is required to validate this relationship with prospectively collected data.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Red blood cell distribution width is associated with mortality risk in patients with acute respiratory distress syndrome based on the Berlin definition: A propensity score matched cohort study

Chen

et al. 2020

Heart & Lung

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“…The dual antioxidant and anti-inflammatory activity of fraxin has been recently demonstrated in a mouse model of acute respiratory distress syndrome (ARDS) [200]. Fraxin inhibited the production of TNF-α, IL-1β, IL-6, ROS, and MDA; suppressed NF-κB, MAPK signaling, and MMP9; and increased SOD in the lung of mice with LPS-induced ARDS [200]. Niu et al reported that fraxin exhibited hepatoprotective effects against CCl 4 -induced liver damage via mitigation of oxidative stress and inflammation [197].…”

Section: Fraxin Fraxin (7-hydroxy-6-methoxy-8-[(2s3r4s5s 6rmentioning

confidence: 99%

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

Hassanein

Sayed

Hussein

et al. 2020

Oxidative Medicine and Cellular Longevity

156

106

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The Keap1/Nrf2/ARE system is a central defensive mechanism against oxidative stress which plays a key role in the pathogenesis and progression of many diseases. Nrf2 is a redox-sensitive transcription factor controlling a variety of downstream antioxidant and cytodefensive genes. Nrf2 has a powerful anti-inflammatory activity mediated via modulating NF-κB. Therefore, pharmacological activation of Nrf2 is a promising therapeutic strategy for the treatment/prevention of several diseases that are underlined by both oxidative stress and inflammation. Coumarins are natural products with promising pharmacological activities, including antioxidant, anticancer, antimicrobial, and anti-inflammatory efficacies. Coumarins are found in many plants, fungi, and bacteria and have been widely used as complementary and alternative medicines. Some coumarins have shown an ability to activate Nrf2 signaling in different cells and animal models. The present review compiles the research findings of seventeen coumarin derivatives of plant origin (imperatorin, visnagin, urolithin B, urolithin A, scopoletin, esculin, esculetin, umbelliferone, fraxetin, fraxin, daphnetin, anomalin, wedelolactone, glycycoumarin, osthole, hydrangenol, and isoimperatorin) as antioxidant and anti-inflammatory agents, emphasizing the role of Nrf2 activation in their pharmacological activities. Additionally, molecular docking simulations were utilized to investigate the potential binding mode of these coumarins with Keap1 as a strategy to disrupt Keap1/Nrf2 protein-protein interaction and activate Nrf2 signaling.

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“…Antioxidants can reduce the severity of ARDS (7). Several kinds of drugs decrease the levels of lipid peroxidation and ROS, attenuate inflammation and oxidative stress, and ultimately alleviate ARDS in mice and improve gas exchange (77)(78)(79)(80). GSH supplementation could significantly alleviate mitochondrial dysfunction and oxidative damage in the LPSinduced ALI model (81).…”

Section: Antioxidantsmentioning

confidence: 99%

The Role of Ferroptosis in Acute Respiratory Distress Syndrome

Zhang

Chen

et al. 2021

Front. Med.

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Ferroptosis is a newly discovered type of regulated cell death that is different from apoptosis, necrosis and autophagy. Ferroptosis is characterized by iron-dependent lipid peroxidation, which induces cell death. Iron, lipid and amino acid metabolism is associated with ferroptosis. Ferroptosis is involved in the pathological development of various diseases, such as neurological diseases and cancer. Recent studies have shown that ferroptosis is also closely related to acute lung injury (ALI)/ acute respiratory distress syndrome (ARDS), suggesting that it can be a novel therapeutic target. This article mainly introduces the metabolic mechanism related to ferroptosis and discusses its role in ALI/ARDS to provide new ideas for the treatment of these diseases.

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Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability

Cited by 27 publications

References 35 publications

Red blood cell distribution width is associated with mortality risk in patients with acute respiratory distress syndrome based on the Berlin definition: A propensity score matched cohort study

Red blood cell distribution width is associated with mortality risk in patients with acute respiratory distress syndrome based on the Berlin definition: A propensity score matched cohort study

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

The Role of Ferroptosis in Acute Respiratory Distress Syndrome

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