Protective effects of Isofraxidin against lipopolysaccharide-induced acute lung injury in mice

Niu, Xiaofeng; Wang, Yu; Liu, Weifeng; Mu, Qingli; Li, Huani; Yao, Huan; Zhang, Hailin

doi:10.1016/j.intimp.2014.12.041

Cited by 62 publications

(35 citation statements)

References 34 publications

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“…Pulmonary edema, an important pathological feature of ALI, could be evaluated by lung W/D weight ratio in animal ALI model [19]. In our present study, SEC or SMC post-intake effectively attenuated pulmonary edema in those mice, which was evidenced by lower W/D weight ratios.…”

Section: Discussionsupporting

confidence: 55%

RETRACTED: Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

Hsia

Yin

2016

Nutrients

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The effects of S-ethyl cysteine (SEC) and S-methyl cysteine (SMC) on lipopolysaccharide (LPS)-induced acute lung injury in mice were examined. Eight hours after LPS challenge, SEC or SMC was supplied in drinking water at 0.5% or 1% for 3 days. LPS increased lung myeloperoxidase activity, neutrophil counts and edema. SEC or SMC post-intake attenuated these events. SEC or SMC suppressed LPS-induced lung expression of cyclooxygenase-2, nuclear factor-κB and mitogen-activated protein kinase, and lowered the generation of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and prostaglandin E2. LPS enhanced the expression of p47phox, gp91phox, Bax and cleaved caspase-3, and increased the production of reactive oxygen species in the lung. SEC or SMC post-intake reversed these alterations. These findings suggest that these agents could protect the lung through their anti-inflammatory, anti-oxidative and anti-apoptotic activities.

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Section: Discussionsupporting

confidence: 55%

RETRACTED: Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

Hsia

Yin

2016

Nutrients

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“…(Gül et al 2012). In macrophages, LPS induction actives transcription of genes encoding proinflammatory proteins, which leads to the release of cytokines and the synthesis of enzymes such as cyclooxygenase-2 (Niu et al 2015). Previous study has shown that LPS increases migration and adhesive properties of esophageal squamous carcinoma cells (HKESC-2 and HKESC-1) by TLR4 stimulation via p38 and selectin, contributing to tumor metastasis (Rousseau et al 2013).…”

Section: Resultsmentioning

confidence: 99%

Effect of LPS on the Viability and Proliferation of Human Oral and Esophageal Cancer Cell Lines

Gonçalves

Cappellari

Santos

et al. 2016

Braz. arch. biol. technol.

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The esophagus and mouth tumors are very frequent malignancies worldwide. Lipopolysaccharides (LPS) are capable of regulating gene expression of pro-inflammatory cytokines by binding to toll-like receptor 4 (TLR4). Recent studies show that LPS can increase the migration ability of human esophageal cancer cell line HKESC-2 by increasing its adhesion properties. However, the effect of LPS has not been tested on viability of human esophageal and oral cancer cells. This study aimed to determine the action of LPS on the cell proliferation and viability in

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“…These excessive inflammatory cytokines and chemokine are important characteristics of ALI [28]. They not only amplify the inflammatory responses and result in inflammatory injury, but also recruit neutrophils into the lung [29–31].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Li‐Fei‐Xiao‐Yan Prescription on Lipopolysaccharide‐Induced Acute Lung Injury via Inhibition of Oxidative Stress and the TLR4/NF‐κB Pathway

Gui

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Li-Fei-Xiao-Yan prescription (LFXY) has been clinically used in China to treat inflammatory and infectious diseases including inflammatory lung diseases. The present study was aimed at evaluating the potential therapeutic effects and potential mechanisms of LFXY in a murine model of lipopolysaccharide- (LPS-) induced acute lung injury (ALI). In this study, the mice were orally pretreated with LFXY or dexamethasone (positive drug) before the intratracheal instillation of LPS. Our data indicated that pretreatment with LFXY enhanced the survival rate of ALI mice, reversed pulmonary edema and permeability, improved LPS-induced lung histopathology impairment, suppressed the excessive inflammatory responses via decreasing the expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokine (MIP-2) and inhibiting inflammatory cells migration, and repressed oxidative stress through the inhibition of MPO and MDA contents and the upregulation of antioxidants (SOD and GSH) activities. Mechanistically, treatment with LFXY significantly prevented LPS-induced TLR4 expression and NF-κB (p65) phosphorylation. Overall, the present study suggests that LFXY protected mice from acute lung injury induced by LPS via inhibition of TLR4/NF-κB p65 activation and upregulation of antioxidative enzymes and it may be a potential preventive and therapeutic agent for ALI in the clinical setting.

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Protective effects of Isofraxidin against lipopolysaccharide-induced acute lung injury in mice

Cited by 62 publications

References 34 publications

RETRACTED: Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

RETRACTED: Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

Effect of LPS on the Viability and Proliferation of Human Oral and Esophageal Cancer Cell Lines

Protective Effects of Li‐Fei‐Xiao‐Yan Prescription on Lipopolysaccharide‐Induced Acute Lung Injury via Inhibition of Oxidative Stress and the TLR4/NF‐κB Pathway

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